cvs Flashcards

Question

Which of the following is a beta-blocker that is contraindicated in slow metabolizers with asthma? Choices A) Atenolol B) Nebivolol C) Propranolol D) Metoprolol XL

Answer 1

C) Propranolol Non-selective B blocker, while others are B1-selective -> can induce bronchoconstriction + Propranolol metabolised by CYP2D6 enzyme -> slow metabolisers of CYP2D6 experience higher drug levels => increased risk of adverse effects (e.g. bronchoconstriction)

Answer 2

**NO** activates **Guanylyl Cyclase** -> converts GTP to **cGMP** -> cGMP then activates myosin light-chain phosphatase (**MLCP**) -> which **dephosphorylates Myosin Light Chain** (MLC) => relaxation of smooth muscle

Answer 3

* main mechanism: REDUCE myocardial O2 **demand** via 1. dilation of SYSTEMIC veins (**venodilation**) -> increase venous capacitance and reduce amt of blood returning to heart => **reduce preload** 2. dilation of SYSTEMIC arterioles (**arteriolar dilation**) -> lower **TPR** => **reduce afterload** * side mechanism: IMPROVE O2 **supply** via **dilation of CORONARY arteries** ## Footnote recall and link to smooth muscle relaxation pathway! nitrates **release NO** -> which activates **Guanylyl Cyclase** -> converts GTP to **cGMP** -> cGMP then activates myosin light-chain phosphatase (**MLCP**) -> which **dephosphorylates Myosin Light Chain** (MLC) => relaxation of smooth muscle

Answer 4

B) Bradycardia nitrates cause hypotension (D) due to its **dilation of systemic blood vessels** (venodilation and arteriolar dilation) -> decreased **preload** and **afterload** -> decreased **SV (and thus CO)** and decreased **TPR** => decreased **BP** which then causes reflex tachycardia (C), not bradycardia as the drop in BP -> activation of **baroreceptor reflex** in carotid sinus and aortic arch -> **sympathetic system** activated -> **increased HR** to compensate for reduced CO | BP = CO (= SV x HR) x TPR ## Footnote headache (A) is due to dilation of **cerebral blood vessels** -> increased intracranial blood volume and **pressure** (increase pressure instead of decrease as **intacranial space is fixed**)

Answer 5

active form -> phosphorylates MLC => contraction of smooth muscle

Answer 6

antagonise **beta-1** adrenergic receptors -> prevent activation of **Gs protein** -> reduce activity of **adenylyl cyclase** -> less conversion of ATP to **cAMP** -> decreased activity of **PKA** -> reduced **phosphorylation of L-TYPE Ca2+ channels**, -> decreased **calcium influx**, which **limits CICR** from **sarcoplasmic reticulum** -> reduce formation of **calcium-calmodulin complex** -> decreased activation of **MLCK** -> reduced **MLC phosphorylation** => decreased contractility of cardiac myocytes | BP = CO (SV x cardiac contractility) x HR

Answer 7

C) CNS effects known as "**B**eta-**B**locker **B**lues", commonly include vivid dreams and clinical depression

Answer 8

nebivolol "newbie-vo**lol**" * B1-selective in low dose * Non-selective in high dose

Answer 9

antagonise **beta-2** adrenergic receptors -> prevent activation of **Gs protein** -> reduce activity of **adenylyl cyclase** -> less conversion of ATP to **cAMP** -> decreased activity of **PKA** -> reduced **inactivation of MLCK** via phosphorylation -> increased **MLC phosphorylation** -> smooth muscle contraction => **bronchoconstriction**

Answer 10

pathway: Ang I converted into Ang II by **ACE** -> **Ang II** binds to AT1 receptors in vascular smooth muscles, causing **vasoconstriction** AND Ang II binds to AT1 receptors and **stimulate aldosterone secretion**, causing **sodium and water retention** * ACEi inhibits ACE -> **less conversion of Ang I to Ang II** -> **lower levels of Ang II** -> less vasoconstriction AND less aldosterone secretion -> less sodium and water secretion * ARB **prevents binding of Ang II to AT1 receptors** -> less vasoconstriction AND less aldosterone secretion -> less sodium and water secretion

Answer 11

1. ACEi **prevent inactivation** of bradykinin 2. accumulation of **bradykinin** 3. (a) irritation of respiratory tract => **dry cough** (b) increase **NO and PG** -> **inflammation**-like responses (e.g. **angioedema**)

Answer 12

Decreased conversion of Angiotensin I to Angiotensin II -> Decreased aldosterone -> Decreased Na+ and H2O retention -> Decreased **BP** and **bloodflow to kidneys** -> Decreased **eGFR** => ACUTE RENAL FAILURE ## Footnote decreased Na+ and H20 retention -> decreased **blood vol** -> decreased **preload** -> decreased **SV** and thus **CO** recall! BP = CO (SV x contractility) x HR

Answer 13

inhibit PCSK9 -> prevent the internalisation and degradation of LDL receptors -> more LDL receptors remaining on liver cells -> increased clearance of LDL from bloodstream => lower LDL levels

Answer 14

patients with **severe** hypercholesterolemia who do not respond well to **statins** ## Footnote usually used when statins alone DO NOT **sufficiently lower** LDL levels (greater LDL reduction when combined due to diff MOA)

Answer 15

patients with hypertriglyceridemias with **VLDL elevation**

Answer 16

inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis => reduce cholesterol synthesis in liver

Answer 17

C) Liver and muscle problems Adverse effects include - myopathy (muscle pain) and rhabdomyolysis (severe muscle breakdown) - elevated liver enzymes

Answer 18

directly inhibit synthesis of triglycerides in liver => reduce VLDL production

Answer 19

D) Treatment of hypertriglyceridemia (Type IV) and of hyperlipidaemia (in combination with statins). Used alongside statins in patients with Familial **Combined** Hyperlipidemia (Type IIb) [high TG and high LDL] when control of TG is insufficient ## Footnote recall! omega-3 acid ethyl esters directly inhibit synthesis of triglycerides in liver => reduce VLDL production treatment of - hyperchylomicronemia: low-fat diets (recall chylomicrons is exogenous source of TG) - familial hypercholesterolemia: statins, PCSK9 inhibitors

Answer 20

D) Treatment of hypercholesterolemia (Type IIa) and of combined hyperlipidaemia (Type IIb) (in combination with niacin). Used alongside niacin in patients with Familial **Combined** Hyperlipidemia (Type IIb) [high TG and high LDL] bcos bile acid binding resins lower LDL while niacin lowers TG ## Footnote niacin (= Vit B3) lower TG levels by reducing release of **fatty acids** into bloodstreams, which are **used by liver** to synthesis TG => reduce **TG synthesis**

Answer 21

C) Constipation. alongside abdominal distension, diarrhoea and flatulence ## Footnote Whether diarrhoea or constipation depends on individuals - diarrhoea due to increased fat content which have a laxative effect (e.g. due to fat drawing water into gut) - constipation due to slowing of gastric emptying, leadin to delayed bowel movements

Answer 22

patients who are allergic to fish as omega-3 acid ethyl esters are derived from fish oil

Answer 23

B) Increased risk of bleeding. as it reduces production of **thromboaxane A2 (TXA2)** which is essential for platelet clotting -> increased bleeding time => special care needed for patients on **anticoagulants** such as aspirin and warfarin ##Footnote recall! NSAIDs are the ones associated with increased risk of gastrointestinal ulcers

Answer 24

D) Injection site reactions, such as redness, swelling, or pain PCSK9 inhibitors are administered via subcutaneous **injection** and thus can cause injection-related adverse effects including above and hypersensitivity reactions ## Footnote recall! liver toxicity and muscle-related side effects both associated with statins

Answer 25

B) Cholesterol synthesis is primarily driven by the body's own production in the evening. Less food consumption and thus **dietary cholesterol** in evening -> body has to **synthesis own cholesterol** ## Footnote HMG-CoA reductase is the rate-limiting enzyme in cholesterol synthesis also means that statins (= HMG-CoA reductase inhibitor) will have greater effect => best taken in evening

Answer 26

are the **ligand** and thus activates **PPAR-a**, a **transcription factor**, resulting in increased expression of genes involved in **lipid breakdown** 1) including **LPL** → increased **hydrolysis** of TG ⇒ decrease in **plasma TG** levels 2) enzymes involved in **FA B-oxidation** pathway (e.g. CPT1) → increased FA B-oxidation → decreased **hepatic** production of **TG** → liver produces and secretes less **VLDL** into blood ⇒ decrease in **plasma TG** levels (since VLDL is **TG-rich**) and decrease in blood **LDL** (since **LDL <- VLDL**) 2) **apolipoproteins** of HDL → increased HDL **synthesis** ⇒ increase in **plasma HDL**

Answer 27

pregnancy, children and teenagers as it **affects neurodevelopment** of fetus and children

Answer 28

gall-stones

Answer 29

bind to **negatively charged** bile acids and bile salts in **small intestine** -> dereased bile acid reabsorption and increased excretion -> liver senses bile acid shortage -> compensates by **converting more cholesterol** into bile acids => decrease in **intracellular [cholesterol]** -> liver upregulates **LDL receptors** to pull more LDL from bloodstream => decrease in **plasma LDL** levels

Answer 30

cholestyramine

Answer 31

bind to **negatively charged** bile acids and bile salts in **small intestine** -> dereased bile acid reabsorption and increased excretion -> liver senses bile acid shortage -> compensates by **converting more cholesterol** into bile acids => decrease in **intracellular [cholesterol]** -> liver upregulates **LDL receptors** to pull more LDL from bloodstream => decrease in **plasma LDL** levels

Answer 32

E) All of the above. Constipation due to resins binding to bile acids -> form insoluble complex -> reduce water content in stool => slow intestinal motility Diarrhoea due to some bile acids left unbound by resins -> undigested bile acids reach colon => draw water into intestines Flatulence due to resins binding to bile acids -> reduce fat digestion ->more undigested fat reaches colon => gut bacteria ferment it and produce gas Impaired absorption due to resins binding to bile acids -> reduce fat digestion (via emulsification, micelle formation and absorption) => reduce absorption of fat-soluble vitamins

Answer 33

inhibits NPC1L1 transporter -> less cholesterol transported from gut into enterocytes (intestinal cells) -> less cholesterol enters bloodstream -> liver responds by increasing LDL receptor expression => lower levels of LDL ## Footnote cholesterol from food and bile absorbed in small intestine -> packaged into chylomictons -> enters circulation

Answer 34

Statins reduce cholesterol production in the liver while Ezetimibe reduces cholesterol absorption in the gut. Thus, combining both targets two sources of cholesterol, leading to a greater LDL reduction ## Footnote ezetimibe + simvastatin = **vytorin**

Answer 35

B) Inhibits platelet activation by increasing cAMP healthy blood vessel -> endothelial cells release **PGI2** -> causing synthesis of **cAMP** via its binding to platelet membrane receptors -> which inhibits release of **granules containing aggregating agents** => prevent platelet activation and aggregation

Answer 36

B) Promotes release of ADP and serotonin blood vessel w/ damaged endothelium -> **exposed collagen fibers** -> thrombin, TXA2 and exposed collagen stimulate platelets to release **arachidonic acid** (AA) from their **membranes** -> AA is converted into **TXA2** (via pathway involving Prostaglandin H2) -> TXA2 binds to specific receptors on **other platelets** -> releasing **aggregating agents** like ADP, serotonin and TXA2 itself => platelet aggregation

Answer 37

acetylates cyclooxygenase (**COX**) => irreversibly **inhibits synthesis** of TXA2

Answer 38

A) Bleeding and C) Gastric upset and ulcers Reduced levels of **PGI2** -> blood vessels do not **dilate** as effectively => **less efficient blood flow** to tissues and thus **slower healing** at injury sites Reduced levels of **PGE2** -> less secretion of **mucus and bicarbonate** -> compromised protective barrier of stomach liming => irritation (gastric upset), mucosal damage and eventual ulcer formation ## Footnote Recall: In the pathway of AA -> TXA2, PGH2 not only forms TXA2, but also PGI2 and PGE2

Answer 39

prevent fibrinogen from binding to GPIIb/IIIa receptors (exposed on platelet surface upon activation) -> prevent formation of bridge bet platelts (cross-linking) => prevent platelet aggregation | fibrinogen -> GPIIb/IIIa receptor occurs during PRIMARY hemostas ## Footnote MOA all slightly diff, with A irreversibly binding receptor (irreversible inhibitor), T reversibly binding to receptor (competitive inhibitor) and E reversibly binding to receptor (competitive mimicker inhibitor)

Answer 40

D) Dipyridamole Dipyridamole **inhibits** phosphodiesterase (**PDE**) enzymes -> inhibit conversion of **cAMP** into 5' -AMP -> increase in intracellular cAMP in platelets -> greater inhibition of the release of **granules containing aggregating agents** => prevent platelet activation and aggregation

Answer 41

D) Tirofiban ## Footnote small molecule, non-peptide agent that competes with fibrinogen to reversibly bind to GPIIb/IIIa receptor

Answer 42

B) Blockade of the ADP receptor inhibit **ADP receptor** on platelets -> prevent ADP-mediated activation of **GPIIb/IIIa receptor** complex -> fibrinogen cannot bind to receptor => inhibit platelet aggregation | fibrinogen -> GPIIb/IIIa receptor occurs during PRIMARY hemostas

Answer 43

B) LMWH primarily targets factor Xa, while unfractionated heparin targets both factor Xa and thrombin. LMWH has a **shorter** chain length -> **lack of binding site** for other enzymes (e.g. thrombin (IIa))

Answer 44

C) Activation of antithrombin III active heparin binds to **ATIII** -> **conformational change** (exposed active site) which allows for **more rapid interaction** ## Footnote for greater inhibition of **thrombin**, heparin must bind to BOTH **ATIII and thrombin** however, for greater inhibition of **factor Xa**, heparin can just bind to **ATIII**

Answer 45

B) LMWH primarily targets factor Xa, while unfractionated heparin targets both factor Xa and thrombin. LMWH has a **shorter** chain length -> **lack of binding site** for other enzymes (e.g. thrombin (IIa))

Answer 46

A) Reduction in cAMP levels through inhibition of adenylyl cyclase

Answer 47

B) To cleave angiotensinogen to form Angiotensin I

Answer 48

D) LMWH has better bioavailability and a longer half-life than unfractionated heparin. longer half-life allows LMWH to be used for long-term prevention and treatment of conditions like deep vein thrombosis (DVT) and pulmonary embolism, as compared to unfractionated heparin which is typically used for acute settings and more intensive treatments, such as in the hospital or during surgeries.

Answer 49

thrombosis and thrombocytopenia **immune-mediated** disorder with formation of **antibodies** against heparin-platelet complex -> activate platelets => abnormal blood clot formation **platelets consumed** in blood clot formation => decrease in platelet count

Answer 50

C) To prevent and treat haemorrhage associated with heparin therapy. Protamine sulfate binds to heparin and neutralises its anticoagulant effects

Answer 51

A) Vitamin K is a **cofactor** in the carboxylation of glutamate residues in clotting factors. => **activtion** of clotting factors ## Footnote (C) is incorrect as vitamin K epoxide is the precursor to vitamin K, and active form of vitamin K is vitamin K hydroquinone

Answer 52

B) Warfarin crosses placenta **readily** and can cause a **hemorrhagic disorder** in fetus

Answer 53

metabolised by cytochrome **P450** => must take note of P450-inhibiting/inducing drugs administered with it (e.g. if P450-inhibiting drug administered with it -> less P450 to metabolise warfarin => overdose of warfarin)

Answer 54

converts plasminogen to plasmin => breakdown of fibrin and fibrinogen itself

Answer 55

link to CVS: atherosclerotic plaque grows and becomes **unstable** -> outer layer **rupture** -> **inner contents** (e.g. cholesterol, lipids and tissue debris) come into contact with blood stream -> trigger **blood clotting** response => blood clot formed can **obstruct blood flow**

Answer 56

angina occurs when there is a **demand-supply mismatch** => aim of treatment: reduce Dd and/or increase Ss - vasodilators **dilate blood vessels** -> increase **blood flow** to heart => improve **Ss** and lower **Dd** - cardiac depressants **reduce HR and contractility** => lower **Dd** * cardiac pacemaker retardants **slows HR** w/o affecting contractility -> improve **Ss** ## Footnote vasodilators lower Dd by - decreasing **preload** via venodilation -> reduced venous returin -> reduced ventricular filling => lower cardiac workload - decreasing **afterload** via arterial dilation -> decrease resistance heart has to pump against => lower cardiac workload cardiac pacemaker retardants improve Ss via lowering HR -> increase **diastolic filling time** -> increased coronary perfusion => improved oxygen supply to heart but doesn't really lower Dd as main factor of Dd is contractility

Answer 57

Lisino**pril**

Answer 58

dry cough ## Footnote due to bradykinin accumulation

Answer 59

CHF progresses, fluid accumulates, causing ventricular and atrial stretch. This stimulates the release of: Atrial Natriuretic Peptide (ANP) from the atria Brain Natriuretic Peptide (BNP) from the ventricles

Answer 60

by * Dilating afferent arterioles → ↑ GFR * Inhibiting renin, aldosterone, and ADH * Increasing Na⁺ excretion in urine ## Footnote does so to **counteract fluid overload**, but it is usually **insufficient** in CHF because ADH, RAAS, and sympathetic activation are more dominant this is bcos CHF patients have persistent low effective circulating volume, so the body **prioritizes water retention (via ADH)** over natriuresis => fluid overload + hyponatremia

Answer 61

C) Tricuspid valve recall that the valves **bet atria and ventricle** are the ones w/ **numbers** => **bi**cuspid (= mitral) and **tri**cuspid

Answer 62

C) Aortic valve * backflow of blood into LV => valve stops blood going **from LV to rest of body** * to do so, blood has to **flow through aorta** => **aortic** valve

Answer 63

* Right * 2nd intercostal space * parasternal

Answer 64

* Left * 2nd intercostal space * parasternal

Answer 65

B) Anchor the atrioventricular valves to the ventricular -> prevent **prolapse** => prevent **regurgitation** | atrioventricular vales = bicuspid (= mitral) and tricuspid valve ## Footnote **papillary muscles** attach chordae tendinae to ventricular walls

Answer 66

* neck * shoulder * medial surface of left arm

Answer 67

* **visceral afferent fibres** (carrying visceral pain) from heart travel **along sympathetic fibres** and enter **spinal cord segments T1-T4** * **somatic sensory fibres** (carrying somatic pain from T1-T4/T5 dermatomes) also enter **spinal cord segments T1-T4** * both nerve fibres enter spinal cord at same level, converge on the **same 2nd order neurons** and are carried up to brain in similar way via **spinothalamic tract** * thus, when **oxygen deficiency** or buildup of **metabolic waste products** **stimulate pain nerve endings** in myocardium, * brain **misattributes** pain coming from visceral afferent fibres as coming from somatic sensory fibres instead * thus, pain from the heart is in correctly perceived by brain as coming from **T1-T4/T5 dermatomes**

Answer 68

* LCA and RCA arise from L and R **aortic sinuses** respectively * which are small **dilations** in **aortic valve cusps** | cusp = leaflet = flap of tissue which open and close in valves

Answer 69

Only during **diastole** * Systole -> **ventricular contraction** -> blood is flowing from LV to rest of body through aorta -> aortic valve is **open** and **blood rushes past** coronary openings * Diastole -> ventricular relaxation -> aortic valve **closes** => blood **backflows** into aortic sinuses and thus into coronary arteries ## Footnote Implication: Tachycardia -> **less time** for **diastole** -> **less time for blood to backflow** into aortic sinuses and thus into coronary arteries (i.e. coronary filling) -> reduced O2 supply to heart muscle => **ischaemia**

Answer 70

LA and LV ## Footnote Circumflex arises from LCA

Answer 71

RCA itself

Answer 72

* RV and LV * 2/3 of IV septum * AV bundle

Answer 73

* marginary artery (AMA): RV * PDA: 1/3 of IV septum (and adjacent portions of ventricles)

Answer 74

* which artery **gives rise to PDA** * usually is **RCA** (85% of the time)

Answer 75

* ***great* cardiac** vein (runs alongside LAD), ***middle* cardiac** vein (runs alongside PDA) and ***small* cardiac** vein (runs alongside AMA) -> drain into **coronary sinus** -> opens into **RA** ## Footnote there are also **anterior cardiac** veins which drain **directly into RA**

Answer 76

branchiocephalic vein, trachea, oesophagus, nerves (vagus, phrenic), thoracic duct, azygos vein ## Footnote branchiocephalic vein @ most anterior trachea posterior to oesophagus vagus and phrenic nerves run alongside oesophagus thoracic duct quite posterior as it is near vertebrae azygos vein @ most posterior

Answer 77

arch of aorta, pulmonary trunk, ligamentum arteriosum, tracheal bifurcation, nerves (vagus and phrenic), thoracic duct, azygos vein ## Footnote arch of aorta @ most anterior ligamentum arteriosum connects arch of aorta to pulmonary trunk thoracic duct quite posterior as they are near vertebrae azygos vein @ most posterior

Answer 78

HEART, great vessels (**S**VC, **A**scending aorta, **P**ulmonary trunk)

Answer 79

oesophagus, thoracic duct, azygos vein, descending aorta, sphlanchic nerves, sympathetic chain ## Footnote descending aorta is now the most posterior blood vessel, sympathetic chain @ most posterior, <- run alongside vertebrae sphlanchic nerves just slightly anterior as they branch off sympathetic chain

Answer 80

* ascending aorta → arch of **A**orta → descending aorta * **B**ranchiocephalic artery (R), L **C**ommon carotid and L **S**ubclavian arteries branch off from arch of aorta * branchiocephalic artery (R) further branches into R **C**ommon carotid and R **S**ubclavian arteries "ABCs"

Answer 81

**deceleration** injury → aorta will **continue to move forward** → but ligamentum arteriosum **holds it** in place ⇒ can cause aorta to **tear**

Answer 82

abnormal opening in **interventricular septum** → blood flows from **higher pressure LV** to **lower pressure RV** ⇒ **left-to-right shunt**

Answer 83

failure of ductus arteriosus to **close after birth** → blood flows from **higher pressure aorta** into **lower pressure pulmonary artery** => **left-to-right shunt** ## Footnote in fetus, ductus arteriosus acts as **shunt** → connects pulmonary artery to aorta → **divert blood** away from non-functional lungs and into systemic circulation upon starting breathing after birth, **increased oxygen levels in blood** triggers ductus arteriosus to **constrict and close** => becomes ligamentum arteriosum

Answer 84

* 4 abnormalities: 1. pulmonary stenosis → increase **RV pressure** 2. thus R ventricular hypertrophy 3. ventricular septal defect → allow **mixing of oxygenated and deoxygenated** blood 4. overriding aorta (where aorta is displaced over VSD, i.e. more to the right) → allow the mixed blood to **enter systemic circulation** * since blood is forced from RV through VSD into aorta ⇒ **right-to-left** shunt

Answer 85

SA node → AV node → bundle of His (AV bundle) → L and R bundle branches → purkinje fibres

Answer 86

ventricular filling occurs in 2 phases * **passive filling** where blood flows passively **from atria into ventricles** due to **pressure gradient**, accounts for **most** of ventricular filling delays electrical transmission, allowing time for * atrial contraction where AV node **delays electrical transmission** -> ensures that **atria contraction** is completed **before ventricles start contracting** => **tops off** ventricles

Answer 87

**fibrous rings** which surround AV valves **separate atria and ventricles** -> ensure that electrical impulses must **go through AV node**

Answer 88

During **phase 0**, upon reaching threshold membrane potential, there is **rapid INFLUX of Na+** through fast voltage-gated **Na+ channels**, causing a **sharp depolarisation** During **phase 1**, there is **EFFLUX of some K+** through **K+ channels**, causing a **small early repolarisation** During **phase 2**, there is efflux of K+ through other K+ channels, but this is countered by the **INFLUX of Ca2+** via **Ca2+ channels**, thus **sustaining depolarisation** (almost like a **"plateau"**) During **phase 3**, there is **EFFUX of K+** through other **K+ channels**, resulting in **repolarisation** During **phase 4**, **K+ leak channels** remain open, keeping the cell at a stable **resting membrane potential**

Answer 89

increased stroke volume, at least until a limit is reached, according to **Starling's law** ## Footnote **strength of contractility** is only affected and in fact regulated by **sympathetic nervous system**, (via **B1**-adrenergic receptors which result in **Ca2+ influx**) NOT by parasympathetic nervous system (only receptors in heart is M2 muscarinic receptors on SA and AV nodes)

Answer 90

by acting directly on **SA node** * Catecholamines (i.e. epinephrine and norepinephrine) -> **activate** *B1-adrenoceptor receptor* * Thyroxine -> enhances **expression** of *B1-adrenoceptor receptor* * Temperature -> higher temp results in faster **SA node firing**

Answer 91

information is sent to **vasomotor centre** (in medulla) -> activates **ANS** * e.g. pain * e.g. **PO2 and PCO2** detected by chemoreceptors * e.g. **BP** detected by baroreceptors

Answer 92

p wave: atrial depolarisation qrs complex: ventricular depolarisation, atrial repolarisation (masked) t wave: ventricular repolarisation ## Footnote q wave: Depolarisation of bundle of His r wave: Depolarisation of right and left bundles s wave: Depolarisation of Purkinje fibres and ventricles

Answer 93

B) RR interval

Answer 94

B) Time for signal to travel from SA node to ventricles (AV nodal delay) measured as BEGINNING of **p wave** to BEGINNING of **qrs complex** ## Footnote **> 0.2s** is abnormal and represents **heart block**

Answer 95

B) Ventricular depolarization and repolarization

Answer 96

300/number of large squares in 1 cardiac cycle | 1 cardiac cycle = e.g. between 2 qrs complexes

Answer 97

ventricular hypertrophy ## * if seen in VT and V6 (lateral) => **L**VH * if seen in V1 and V2 (septal) => **R**VH

Answer 98

**partial occlusion** or reduction of blood flow in coronary artery -> **subendothelial** infarct -> where only **inner layers** of heart muscle is affected => myocardial **ischaemia** esp if many leads involved ## Footnote if **localised** to a few leads -> can be a **reciprocal** change opp to **ST elevation** seen in MI (just rmb as I ↔ II and III aVL ↔ aVF)

Answer 99

**complete occlusion** of coronary artery -> **transmural** infarct -> where **all layers** of heart muscle is affected => myocardial **infarction**

Answer 100

av**R** = towards **R** arm (i.e. current heading there is (+)) av**L** = towards **L** arm (i.e. current heading there is (+)) av**F** = towards **F**oot (i.e. current heading there is (+))

Answer 101

V1, V2 these 2 are the most "middle" alr

Answer 102

none! must look for reciprocal changes in leads V1-4 | V3 and V4 correspond to anterior area of heart

Answer 103

I, aVL, V5, V6 * aV**L** points towards **L** arm * lead I also points towards **L arm** * V5 and V6 are the most **"Left"** out of V leads | **L**ateral = **L**eft side of heart

Answer 104

II, III, aVF, * aV**F** points towards **F**eet * lead II and III also points towards **F**eet | in**F**erior = towards **F**eet (i.e. lower body)

Answer 105

* septal (V1, V2) recall that LAD supplies 2/3 of septum * anterior (V3, V4) V3 and V4 covers area only slightly to left of septum

Answer 106

**L**ateral (I, aVL, V5, V6) since leads are towards **Left** and are towards *many different directions*

Answer 107

inferior (II, III, aVF)

Answer 108

closure of **aortic** valve (due to **ventricular pressure dropping below pressure in aorta**) -> triggers **isovolumetric relaxation** -> where ventricles relax in a **closed chamber** (i.e. both valves are closed) -> resulting in **pressure dropping rapidly** w/ no change in volume

Answer 109

start of **filling** phase of diastole happens when **pressure in LV < LA** -> mitral valve opens -> **volume increases** w/ only slight increase in pressure

Answer 110

closure of **mitral** valve -> triggers **isovolumetric contraction** -> where ventricles contract in a **closed chamber** (i.e. both valves are closed) -> resulting in **pressure increasing rapidly** w/ no change in volume

Answer 111

start of **ejection** phase of systole happens when **pressure in LV > aorta** -> aortic valve opens -> **volume decreases** but pressure continues to increase initially, before gradually decreasing ## Footnote at first, **rapid ejection**: **ventricles contract** forecefully -> eject large vol of blood into aorta => pressure still increasing then, **reduced ejection**: **venticle contraction weakens** -> blood still pushed out due to **mometum from high-speed blood flow** => pressure plateaus and starts decreasing

Answer 112

* S1: closure of mitral valve * S2: closure of aortic valve ## Footnote since closure of mitral valve = start of ventricular systole and closure of aortic valve = start of ventricular diastole => time from s1 to s2 = systole and time from s2 to s1 = diastole

Answer 113

due to **rapid** flow of blood **from atria to ventricles** -> occurs during **passive filling** of ventricles => **early diastole** (soon after s2)

Answer 114

due to **stiffening of ventricles** (e.g. from ventricular hypertrophy) -> atria needs to **contract harder** to **complete filling** of ventricles => **late diastole** (before S1)

Answer 115

* inspiration **lowers intrathoracic pressure** (recall: diaphragm and chest muscles contract -> increase in intrathoracic volume => decrease in intrathoracic pressure) -> larger **pressure gradient bet systemic veins and RA** (since RA is **inside thorax** and systemic veins are not) -> increase in **venous return** to RA -> **more blood** enters RA and thus later RV -> RV **takes longer to eject blood** -> PULMONARY valve **closes later than usual** * expansion of lungs result in expansion of alveolar capillaries -> blood pooling in **pulmonary veins** -> **less blood** return to LA and thus fill LV -> LV doesn't need as much time to **eject blood** => AORTIC valve closes earlier than normal * **inspiration** -> difference in closure of pulmonary and aortic valves => **split S2** (into A2 and P2)

Answer 116

* young people * athletes

Answer 117

when there is a **septal defect** (specifically **atrial septal defect (ASD)**) that results in **L-to-R shunt** -> **more blood in RA (and RV)** and **less in LA (and LV)** -> pulmonary valves closes later and aortic valve closes earlier => S2 split into A2 and P2

Answer 118

time with carotid **pulse** * Diastolic (S2): occurs **after** carotid pulse * **S**ystolic (**S**1): occurs **coincident with** carotid pulse

Answer 119

systole * bcos that is when **ventricles contract** -> blood moves from RV to lungs through pulmonary artery and LV to rest of body through aorta -> and thus have to **pass through pulmonary valve and aortic valve** * thus if valves are **narrowed** -> blood has to **forecfully pass through** during systole => murmur | **mid**-systolic (crescendo-decrescendo)

Answer 120

diastole * bcos that is when **ventricles relax** and blood is already in aorta and pulmonary artery * thus if valves are **incompetent** -> blood **leaks back** from blood vessels into ventricles => murmur | **early** diastole

Answer 121

diastole * bcos that is when **ventricles relax** -> blood from atria fill ventricles -> and thus blood have to pass through mitral valve * thus if mitral valve is **narrowed** -> blood has to **forecfully pass through** (via atria contracting harder to force blood) => murmur ## Footnote **mid-to-late** diastole bcos murmur happens **during atria contraction** diastole = passive filling (at start) + atria contraction (**towards end**)

Answer 122

systole * bcos that is when **ventricles contract** while **atria relaxes** -> blood is already in ventricles * thus if mitral valve is **incompetent** -> blood is **pushed back into LA** instead of being ejected into aorta => murmur ## Footnote **pan**-systolic

Answer 123

* arise from **internal** jugular vein * reflect changes in **RA pressure** ## Footnote internal and external jugular vein -> subclavian vein -> branchiocephalic vein -> SVC => RA

Answer 124

A) **a**trial contraction ## Footnote recall that ventricular filling (during diastole) = passive filling + atria contraction => thus a wave always after y descent

Answer 125

B) Atrial rela**x**ation

Answer 126

B) Atrial filling from the **v**ena cava

Answer 127

B) Passive filling of the ventricles ## Footnote recall that ventricular filling (during diastole) = passive filling + atria contraction => thus y desent always before a wave

Answer 128

RV hypertrophy or tricuspid stenosis -> increase in **pressure needed to fill RV** -> increase in **strength of atria contraction** and thus increase in pressure in RA => bigger a wave

Answer 129

tricuspid regurgitation * if coincident with **ventricular contraction** cos that is when **tricuspid valve closes** to prevent backflow of blood * thus if tricuspid valve is **incompetent** -> **blood flows back into RA** instead of going into pulmonary artery during systole -> **more blood** in RA -> **increase pressure** in RA => bigger v wave

Answer 130

CO = stroke volume x heart rate * preload = **volume** of blood in ventricles at **end of diastole** thus more blood in ventricles -> **more blood** to be pumped out => increase stroke volume * afterload = **resistance** heart must overcome to **eject blood during systole** thus increased resistance -> **harder for ventricles to pump blood out** => decrease stroke volume * contractility increased contractility -> stronger, more forceful contractions -> **more blood can be pumped out** => increase stroke volume

Answer 131

BP = CO (stroke volume x heart rate) X TPR | TPR = total peripheral resistance

Answer 132

stroke volume/end-diastolic volume x 100% ## Footnote stroke vol = end systolic vol - end diastolic vol

Answer 133

* Heart Failure with Reduced Ejection Fraction (HFrEF): EF < 40% * Heart Failure with Preserved Ejection Fraction (HRpEF): EF > 50% | normal EF = 55-75%

Answer 134

**LV** becomes **weak or damaged** -> **pump function** is impaired (i.e. **much less blood** is ejected with each heartbeat) | common causes include MI and HTN

Answer 135

**LV** becomes **stiff and thickened** -> does not **relax and fill** as well -> **less overall blood** being pumped out even though pumping function is normal | common cause: LVH

Answer 136

heart damage (**ischaemic** injury) -> **decreased contractility** -> decrease in CO and SV -> body responds by **activating SNS** (i.e. adrenergic stimulation) and inactivating PNS => **increase HR and contractility** which increases CO, but also **excessive sweating** due to activation of sweat glands

Answer 137

* forward failure due to **reduced stroke volume** => **hypotension** => **decreased organ perfusion** also leads to **activation of RAAS** -> increases **Na+ and H2O retention** and thus further exacerbates **pulmonary oedema** * backpressure due to **blood backing up** into LA and pulmonary circulation -> PULMONARY venous **hypertension** and PULMONARY **oedema** => breathlessness on exertion, orthopnoea, paroxysmal nocturnal dyspnoea

Answer 138

decrease in **LV ejection fraction** causes blood to pool in L side of heart -> increase in pressures of LV and LA -> increase in pulmonary venous pressure -> **increase capillary pressure**, which is the major Starling force favouring filtration of fluid into the pulmonary interstitium -> when filtration of fluid **exceeds the capacity of pulmonary lymphatics** to remove the fluid => pulmonary oedema ## Footnote must write that capillary pressure is the "**major Starling force** favouring filtration of fluid into the pulmonary interstitium" in exams

Answer 139

**fluid** in lungs -> **hinders efficient exchange** of O2 and CO2 -> **V/Q mismatch** where there is perfusion but poor ventilation => **shunt** ## Footnote must write that capillary pressure is the "**major Starling force** favouring filtration of fluid into the pulmonary interstitium" in exams

Answer 140

increased O2 consumption and CO2 production during exertion -> **increased ventilatory demand** -> inability of lung to respond to increased demand due to **reduction of gas exchange** by **pulmonary congestion** => dyspnoea | 1st to develop (early symptom)

Answer 141

lying down position -> gravity no longer helps pool blood in legs -> increased venous return to heart from lower limbs -> overload on LV (preload) -> back pressure effect in lungs -> pulmonary congestion => dyspnoea | Last to develop (SNS not working anymore) ## Footnote when standing up -> blood pools in legs again -> load on heart is removed -> back pressure effect on lungs is eased -> pulmonary congestion relieved => dyspnoea improves

Answer 142

patient lies down to sleep -> pulmonary congestion through same mechanism as orthopnoeasame as orthopnoea -> but patient is still awake, so **sympathetic activation** is **adequate to compensate** -> however, when patient goes to **sleep**, **sympathetic activity is reduced** -> pulmonary congestion continues until **breathing is compromised** -> patient wakes up breathless, and **sits or stands up** -> results in activation of sympathetic system again and blood pooling in legs -> pulmonary congestion relieved and patient feels better | 2nd to develop (SNS still working to counter it)

Answer 143

D) All of the above * Hepatosplenomegaly (A) occurs as RHF results in **blood backing up into venous system** (i.e. SVC and IVC and beyond) -> increased **venous pressure** => hepatic congestion and splenic enlargement * Ascites and pedal oedema occur as RHF reult in **blood backing up into venous system** (i.e. SVC and IVC and beyond) -> increased **venous pressure** -> increased **hydrostatic pressure** in systemic and abdomina **capullaries** => oedema

Answer 144

LHF results in **blood backing up into pulmonary circulation** -> increased pressure in pulmonary circulation -> increased **hydrostatic pressure** in **pulmonary capillaries** -> **fluid forced out into alveoli** -> alveoli **collapse** -> however during inspiration, **air forces alveoli open** => alveoli **snapping open** causes a **crackling** sound ## Footnote why collapse? recall! **surfactant** produced by type 2 pneumocytes helps to **dispel fluid molecules** lining alveoli -> lowers **surface tension** which would otherwise cause alveoli to collapse

Answer 145

inhibitory when BP increases -> baroreceptors are **streched more** -> **increased firing** of INHIBITORY impulses -> **REDUCES sympathetic outflow** -> decrease in **HR and cardiac contractility** (=> decrease in **CO**), as well as results in **vasodilation** (=> decrease in **TPR**) => thus decrease in BP

Answer 146

arterial pressure is insufficient to **maintain perfusion**

Answer 147

* related to activation of SNS: sweating, skin being pale and cold to touch * renal-related (and secondary RAAS activation): decreased urine output ## Footnote skin being pale and cold to touch is due to vasoconstriction which helps to increase TPR and thus increase BP

Answer 148

* hypovolaemic shock * cardiogenic shock * obstructive shock * distributive shock (sepsis, anaphylaxis, neurogenic)

Answer 149

elderly due to **degeneration** of **baroreceptor reflexes**

Answer 150

D) all of the above * CKD (A) results in decreased GFR -> impaired filtration of sodium and water => **sodium and water retention** -> lower sodium levels detected by MD -> triggers JG cells to release renin => activation of **RAAS** * aortic coarctation (B) is **congenital narrowing of aorta** -> increased **TPR** => HTN * renal artery stenosis (C) results in **decreased blood flow to kidney** -> kidney **misinterprets as low BP** and compensations by trying to increase BP through **activation of RAAS**

Answer 151

**endothelial injury** caused by the 4 modifiable **risk factors** * HTN * dyslipidemia * diabetes * tobacco smoking | basically **3 gao + 1** ## Footnote 3 non-modifiable risk factors: * age * sex * genetics (ethnicity)

Answer 152

soft yellow lipid core, w/ **thick** white **fibrous cap** ## Footnote in contrast, unstable plaque has **large lipid core** w/ **thin fibrous cap**

Answer 153

* aneurysm and aortic dissection due to high BP -> increases **force exerted on arterial walls** -> **progressive damage** which weakens **tunica media** of aorta => **dilation** of vessel, resulting in aneurysm OR **tunica intima tearing**, resulting in **blood entering** vessel wall layers and thus **splitting them apart**, resulting in dissection * heart-related (e.g. (concentric) hypertrophy of LV, HF, IHD, etc) | i.e. **mechanical stress** weakening tunica media ## Footnote covers ALL types of blood vessles * aneurysm happens in **biggest vessel** = aorta * atherosclerosis happens in **large vessels** incl coronary arteries * arteriolosclerosis happens in **small vessels**

Answer 154

A) Atherosclerosis due to plaque formation -> loss of **structural integrity** of arterial wall (degeneration of tunica media) => **dilation** of vessel | i.e. **ischaemic damage** to tunica media ## Footnote different mechanism from HTN, only thing same is layer affected

Answer 155

pulsatile abdominal **mass** bcos most common site of aneurysm is **abdominal aorta**

Answer 156

* **sharp** shooting pain between the **scapulae** * sudden severe **stomach** pain | both are due to dissection in **descending** aorta ## Footnote however, most common site of dissection is ASCENDING aorta

Answer 157

cardiac tamponade (haemopericardium) where a dissection in **ascending aorta** where tear involves ALL layers of aorta -> blood can now **flow into pericardial space** -> **accumulation** of blood -> **increases pressure on heart** -> reduce heart's ability to **expand fully** -> reducing its **SV** and thus **CO** (since CO = SV x contractility)

Answer 158

Beck triad * hypotension due to blood being unable to **pump effectively** -> reduced **SV** and thus **CO** (BP = CO x HR) * distended neck veins due to heart being unable to **pump effectively** -> blood **backs up into venous system** => increased pressure in venous system and thus **increased JVP** * distant heart sounds due to **accumulation of blood **in pericardium **dampening** heart sounds

Answer 159

high **troponin** levels as troponin is a protein found in **heart muscle cells** -> **released into bloodstream** when heart muscle is **damaged** | either I or T but usually T cos Troponin **T** = heart a**TT**ack ## Footnote troponin plays a critical role in **muscle contraction**

Answer 160

* arises with **exertion** * relieved by **rest** or **nitroglycerin** ## Footnote pain is predictable (i.e. occurs with **similar levels of exertion**) bcos chest pain only occus when **exertion increases myocardial O2 demand**, resulting in it **exceeding supply** which has been **reduced** due to **FIXED atherosclerotic narrowing** of coronary arteries

Answer 161

* chest pain that occurs even at **rest** or with **minimal exertion** OR increased severity, frequency or duration of chest pain * relieved only by **nitroglycerin**, but **not as effectively** (as stable angina)

Answer 162

**stable plaque**, no rupture ## Footnote recall! histological finding is soft yellow lipid core w/ **thick white fibrous cap**

Answer 163

**unstable** plaque -> **rupture** -> formation of **thrombus** which **partially occludes** coronary artery ## Footnote recall! histological finding of unstable plaque is large lipid core w/ **thin fibrous cap**

Answer 164

B) Stable angina which has turned into unstable angina bcos **troponin levels not affected** => **unstable** angina

Answer 165

acute **retrosternal** chest pain w/ **radiation** to left shoulder and arm | retrosternal = behind sternum (relate to retroperitoneal kidneys)

Answer 166

* **A**lveolar oedema, leading to **B**ilateral perihilar shadowing (**B**atwing opacities) * Kerley **A** & **B** lines (Interstitial oedema) * **B**lunting of costophrenic angle (Pleural effusion) * **C**ardiomegaly * **D**ilated pulmonary vessels <- pulmonary venous congestion * Upper lobe **D**iversion <- increased visibility of upper lobe veins (which are usually smaller than lower lobe veins) <- pulmonary venous pressure forcing blood upwards

Answer 167

**coagulative** necrosis bcos of **ischemia** in organs ## Footnote recap! histological/microscopic findings: * **'ghost cellular outlines'** (i.e. cell structures present without nucleus) <- denaturation of structual proteins BEFORE enzymatic digestion * **eosinophilic** and **amorphous** cytoplasm <- denaturation of structural proteins => denatured proteins **stain pink** => result in **lack of structure** * **neutrophil** invasion <- to **remove dead cells**

Answer 168

* **0-12h: NOT VISIBLE** * 12-24h: mottling, **botchy discolouration** * 24-72h: pale **yellow** * 3-10 days: **hyperemic border** around pale yellow area (**reddish** area due to reperfusion) * 6-8 **WEEKS**: **fibrous SCAR**

Answer 169

* **0-12h: NOT VISIBLE** * 12-24h: eosinophilic and loss of nuclei (both due to **coagulative necrosis**), interstitial **oedema** (due to increased capillary permeability and increased plasma hydrostatic pressure) * **24-72h: NEUTROPHIL INFILTRATION** * 3-10 days: **granulation tissue** starts forming * 6-8 weeks: **fibrous SCAR**

Answer 170

* first 24 hrs: IMMEDIATE AFTERSHOCK (castle trembles -> electrical failure) **ventricular fibrillation/tachycardia** ("power system fails") -> **sudden cardiac death** * 1-3 days: BURNING RUINS (smoke and fire around castle walls) **inflammation** (involves neutrophil infiltration) -> spread of inflammation from myocardium to pericardium => **fibrinous pericarditis** * 3-10 days: STRUCTURAL COLLAPSE (weakest point) **ventricular wall rupture** ("outer wall collapses") -> **cardiac tamponade** **intraventricular septum rupture** ("inner wall collapses") -> **shunt** formation * weeks to months: RECONSTRUCTION ventricular wall undergoes fibrosis -> weakened -> dilation/bulging of walls => **ventricular aneurysm** ("rebuilt walls are not as strong and can't take the stress") **autoimmune pericarditis** => Dressler syndrome ("castle's defenses turn against itself)

Answer 171

C) 2-3 Days formation of **granulation tissue** (3-10 days after onset) -> **NOT as organised** -> thus does NOT have same **tensile strength** as normal myocardium or collagen scar and is **at its weakest** => highest risk of **ventricular rupture** | thus ventricular rupture is an **early complication** of AMI

Answer 172

Strep pyogenes

Answer 173

happens **1-3 weeks AFTER** strep infection -> **M** protein of GAS resembles human cardiac **M**yosin (**M**olecular **M**imicry), resulting in **antibodies cross-reacting w/ self-antigens**, -> causing damage to tissues, in particular **fibrosis of heart valves** -> predispose to **infective endocarditis**

Answer 174

type 2 (i.e. type **B**) bcos molecular mimicry -> anti**B**odies targeting self-tissues

Answer 175

A. Mitral valve ## Footnote options are actually arranged from most commonly to least commonly affected

Answer 176

* DHP: primarily act on **vascular smooth muscle** -> mainly **vasodilation** * non-DHP: act on both vascular smooth muscle and **cardiac conduction system** -> mainly **reduced HR and contractility**

Answer 177

* vera**p**amil * **di**ltiazem "like you broke up the **dipine** in DHP CCBs" ## Footnote verapamil > diltiazem as cardiac depressant "**very**-pamil bcos it is **very** strong"

Answer 178

* amlo**dipine** * nife**dipine** ## Footnote nifedipine > amlodipine as anti-hypertensive

Answer 179

block **Na+** channel -> slows phase **0** depolarisation "**salty** CAB driver gets **0** dollars" ## Footnote CAB bcos there is class 1**C**, 1**A** and 1**B** more legit recall! phase 0 depolarisation is due to Na+ influx as Na+ channels open

Answer 180

**beta** blockers -> reduces phase **4** depolarisation "beta has 4 letters"

Answer 181

block K+ channel -> prolongs phase **3** repolarisation ## Footnote e.g. amiodarone recall! phase 3 repolarisation is due to K+ influx as K+ channels open

Answer 182

**non-DHP** CCB -> prolong phase **4** depolarisation

Answer 183

E. By suppressing the sympathetic nervous system's response to low blood sugar Drop in blood glucose levels -> activation of **SNS** -> symptoms including tremors, sweating and palpitations -> serve as **warning signs**

Answer 184

aspirin as it prevents **initial step** of platelet aggregation -> lowers **risk** of clot formation ## Footnote by inhibiting COX-1, which is responsible for producing TXA2, potent promoter of platelet aggregation

Answer 185

platelet GPIIb/IIIa receptor blockers as it blocks **final step** in platelet aggregation -> **prevent** clot formation

Answer 186

thrombolytics as it dissolves fibrin (protein that holds clot together0 => thus **dissolves clot**

Answer 187

inhibition of cardiac pacemaker **I(f) current** (i.e. funny current) -> reduction in cardiac workload => reduction in myocardial O2 **demand** | I(f) current in SA node

Answer 188

* **visual** problems (luminous phenomena) * bradycardia (and associated symptoms)

Answer 189

* **B**eta-blockers * **C**ardiac glycosides * **D**iuretics (loop and potassium-sparing) * **N**itrates * **H**ydralazine * **S**acubitril-Valsartan **"BCD n Hs"** ## Footnote difference from treatment for HTN: - **A**CEi and ARB not commonly used (replaced by Sacubitril-Valsartan) - **C** stands for **C**ardiac glycosides, not **C**CBs - **N**itrates, **H**ydralazine and **S**acubitril-Valsartan used

Answer 190

* beta-1 selective: bisoprolol, metoprolol XL * non-selective: carvedilol * mixed: nebivolol ## Footnote not approved are **PAP**: **P**ropranolol, **A**tenolol, **P**indolol

Answer 191

* sacubitril: inhibits **neprilysin** -> thus inhibits **breakdown of ANP and BNP** => **prolongs** BNP effects of vasodilation, natriuresis and diuresis * valsartan (AT1 blocker / ARB): **blocks Ang II action** => reduce vasoconstriction and aldosterone secretion ## Footnote valsartan is needed as **neprilysin also breaks down Ang II** => inhibition of Ang II results in less breakdown of Ang II and thus more Ang II

Answer 192

* hyperkalaemia * **renal failure**

Answer 193

* **aminoglycosides** <- both have adverse effect of **ototoxicity** * NSAIDs ## Footnote * recall! ami**NO**glycosides has adverse effects of **N**ephrotoxicity and **O**totoxicity * recall! NSAIDs reduce prostaglandin synthesis -> decrease in vasodilation of afferent arteriole -> reduction in renal blood flow

Answer 194

hyperaldosteronism

Answer 195

* spironolactone: gynecomastia * triamterene: kidney stones, acute renal failure

Answer 196

**selectively dilates arterioles** (arteriolar dilation) -> decrease in systemic vascular **resistance** (SVR) => reduced **afterload**

Answer 197

* symptoms associated with baroflex associated sympathetic activation (e.g. flushing, hypotension) * hydralazine-induced **lupus** syndrome (HILS)

Answer 198

inhibits Na+-K+ exchange -> increases **[Na+]** -> increased Na+ leads to less **Ca2+ efflux** -> greater [Ca2+] results in increased cardiac **contractility** -> increased **CO** (since CO = SV x HR and contractility affects SV) -> leads to 2 effects: 1. decrease in **sympathetic tone** -> reduced vasoconstriction of systemic veins (**venoconstriction**) -> less blood returning to heart => reduced **PRELOAD** 2. increased **renal blood flow** -> reduced **renin** release -> reduced production of **Ang II** -> less vasoconstriction of arterioles (**arteriolar constriction**) -> decrease in **SVR** => reduced **AFTERLOAD**

Answer 199

* **atrial fibrillation** due to digitalis reducing sympathetic tone -> increase **parasympathetic** activity => slows **AV conduction** * systolic dysfunction | AF = **rapid**, irregular atrial impulses that bombard **AV node**

Answer 200

high intracellular **Ca2+** -> increased **automaticity** => progressively more severe **dysrhythmia** (AV block, AF, VF) | overload of electrical impulses -> overwhelm AV node -> functional block

Answer 201

1. **discontinue cardiac glycoside** therapy 2. correction of K+ or Mg2+ deficiency (as hypokalaemia and hypomagnesemia -> increase binding of digitalis to Na+-K+ ATPase) 3. **anti-arrhythmic** drugs, particularly **lidocaine** (class Ib) and **propranolol** (class 2) 4. digoxin antibody (bind to plasma digoxin -> form complexes that are excreted renally) ## Footnote recall! * class I, **3 subclasses**, **sodium** channel blocker, phase **0** depolarisation "**CAB** driver **salty** bcos he got **0** dollars" * class 2, **beta** blockers, phase 4 depolarisation "beta has **4 letters**, thus phase **4** depolarsiation + used for **AFib**"

Answer 202

* congenital **narrowing** (stenosis) of aorta * defining characteristic: **higher BP** (hypertension) in **upper body**, **lower BP** (hypotension) in **lower body** => **radio-femoral delay**

Answer 203

macrophages containing **haemosiderin** as LHF -> pulmonary congestion and **microhemorrhages** in alveoli -> macrophages **ingest RBCs** and break them down => presence of haemosiderin (**product of Hb breakdown**)

Answer 204

* **left** * 5th intercostal space * **lower sternal border** ## Footnote it's the odd one out in comparison, mitral (bicuspid) valve is best heard * left * 5th intercostal space * midclavicular line

cvs Flashcards

(233 cards)