1
Q
four types of shock
A
hypovolemic shock cardiogenic shock distributive shock obstructive shock
2
Q
hypovolemic shock
A
caused by blood loss, burns, blood loss, diarrhea
3
Q
cardiogenic shock
A
caused by reduced output, pump failure (MI)
4
Q
distributive shock
A
caused by anaphylaxis, septic shock, neurogenic shock, all of these cause excessive vasodilation need volume
5
Q
obstructive shock
A
caused by pulmonary embolism cardiac tamponade tension pneumothorax (collapsed lung)
6
Q
shock
A
circulatory insufficiency that creates imbalance between tissue O2 supply and demand causing reduction in effective tissue perfusion and suboptimal substage
7
Q
which hormone is produced at higher levels during shock
A
epinephrine reinforces adrenergic tone early stages, then it is reduced after BP is restored
8
Q
first compensatory mechanism in shock
A
increase cardiac output in response to insufficient oxygen supply
9
Q
if increased CO is inadequate… (shock)
A
amount of O2 extracted from Hg by tissues is increased, decreased SVO2
10
Q
6 main steps in shock response
A
- stimulation of carotid baroreceptor stretch relax activates sympathetic NS leading to arterial vasoconstriction = redistribution of blood flow from skin, skeletal muscle, kidney, and splanchnic viscera 2. increase heart rate and contractility causing increase CO 3. venous constriction augments venous return 4. release of vasoactive hormones to increase arteriole and venous tone 5. release of ADH enhances water retention 6. activation of RAAS enhances Na, H20 retention
11
Q
3 stages of shock
A
pre shock shock end organ dysfunction
12
Q
edema
A
accumulation of fluid in interstitial tissues ex: pleural effusion and ascites results from disturbance of ECF circulation bt capillaries and interstitial space
13
Q
factors that regulate edema
A
- capillary hydrostatic pressure 2. capillary permeability 3. osmotic pressure 4. lymphatic channels
14
Q
capillary hydrostatic pressure
A
force pushing fluid from capillaries into extracellular space
15
Q
capillary permeability
A
determines ease of fluid flow through capillary endothelium
16
Q
osmotic pressure
A
water attracting proper exerted by proteins in blood that attract fluid from interstitial space back to the capillaries
17
Q
lymphatic channels
A
collect fluid forced out of capillaries by hydrostatic pressure and return fluid to circulation
18
Q
pathogenesis of edema
A
- increased capillary permeability (swelling and acute inflammation) 2. decreased intravascular oncotic pressure (due to low plasma proteins, via kidney dx, malnutrition, liver dx) 3. increased hydrostatic pressure (heart failure)
19
Q
arterial thromboembolic dx main cause
A
injury to vessel wall via arteriosclerosis ulceration and rupture of cholesterol plaque
20
Q
cardioembolic sources of a clot
A
within atrial appendages (potential space) surface of heart valves (valve vegetation/endocarditis) wall motion defect (mural thrombus caused by MI or Afib)
21
Q
thrombus
A
intravascular clot occurring at site of tissue injury can occur at any vessel (arterial or venous)
22
Q
emboli
A
detached clot or cholesterol plaque carried into pulmonary or systemic circulation plugs smaller vessel, blocking blood flow and causing necrosis
23
Q
Virchow’s triad
A
- slowing or stasis of blood flow 2. blood vessel wall damage 3. increased coagulability of blood
24
Q
what might form emboli besides blood
A
malignancy, fat, air, amniotic fluid, foreign particles, sepsis
25
malignancy thrombosis
caused by 3 main things 1.rapid release of thromboplastic materials during treatment 2. platelets and coagulation factors consumed faster than replenished 3. large tumor releasing thromboplastic materials
26
fat embolism
caused by severe bone fracture disrupts fatty bone marrow and adipose tissue emulsified fat globules get sucked into being and carried to lungs
27
air embolism
large amounts of air get sucked into circulation could be from lung injury or or accidentally injected into circulation (IV)
28
amnionic fluid embolism
fluid entered circulation through tear in fetal membrane which then blocks the maternal pulmonary capillaries the material in fluid also activates coagulation mechanisms causing coagulation syndrome
29
foreign particulate matter embolism
particulate matter may injected by substance users that crush and dissolve tablets for oral use
30
septic emboli
infectious endocarditis lesions or with local infections causing thrombosis due to inflammation that are secondarily infected and embolize
31
predisposing factors to DVT
prolonged immobilization (which causes Virchows triad) impaired milking action of leg musculature that normally promotes venous return and stasis of blood veins preventing of normal emptying
32
if a DVT breaks from the vessel wall...
it can travel through the blood stream and lodge into the lungs, causing a pulmonary embolism
33
large pulmonary emboli
complete blockage of main pulmonary artery or major branches obstructing blood flow to lungs
34
consequence of large PE?
right side of heart is distended pulmonary a. is congested with blood, increasing pulmonary pressure poor supply to LV, unable to pump adequate blood to brain and other vital organs systemic pressure falls and may go into shock
35
how do you diagnose a PE?
contrast CT of chest can do VQ scan
36
treatment of PE
anticoagulation drugs unfractionated heparin, LMWH, warfarin
37
heart is no longer able to pump adequate amounts of blood
heart failure
38
diastolic heart failure
filling problem impaired diastolic relaxation most often caused by ventricular hypertrophy or from poorly controlled HTN or stenotic valve dx usually first
39
systolic heart failure
contracting problem impaired squeezing function of heart caused by ischemic heart disease regurgitation of heart disease
40
frank starling mechanism
elasticity decrease with failure
41
compensated heart failure
heart muscles will stretch and increase force of contraction to pump blood some stretch left patients can be asymptomatic
42
decompensated heart failure
diminishing return on hearts ability to stretch and forcefully pumping blood from heart no stretch at all symptomatic
43
aortic aneurysm
dilation or out poaching of portion of arterial wall caused by atherosclerosis, HTN, or congenital weakness
44
aortic dissection
blood is forced into middle layer of artery false lumen tears as it blood volume two types: Ascending and Descending
45
coarctation of aorta
congenital band of fibrous tissue after take off of major branches to upper extremities
46
where is a coarctation typically found ?
at the isthmus (close proximity to left subclavian artery)
47
PDA
patent ductus arteriosus narrowing severe enough that it is dependent on this neonatal artery once this closes, infants develop heart failure and shock
in coarctation, blood is able to move around/compensate but this closes = low blood supply
48
physical exam of coarctation
femoral pulse is weak or absent systolic HTN in upper extremities more common in males than females
49
treatment of coarctation
continuous IV infusion of prostaglandin E1 (alprostadil) to vasodilator and maintain ductus arterioles dopamine/dobutamine to improve contractility of those with heart failure surgical pair
50
types of cardiomyopathy
dilated cardiomyopathy hypertrophic cardiomyopathy
51
dilated cardiomyopathy
enlargement of heart and dilation of chambers impaired action leads to chronic heart failure
52
hypertrophic cardiomyopathy
marked hypertrophy of heart muscle , muscle fibers in disarray this then reduces the size of the ventricles (then non compliant in diastole) LV flows into the aorta, thick septum impinges mitral valve, blocking outflow from ventricles heart is unable to fill like it should
53
most common cause of valvular heart disease
degeneration
54
infective endocarditis
more common in persons with altered anatomy and hemodynamics inciting events include: poor dental health, incisive procedure, prosthetic heart valves, IV drug abuse
55
rheumatic heart disease
less common, patients with untreated strep infection causing inflammation damage to the mitral valve
56
mitral valve prolapse
one of the leaflets enlarge, stretch, and prolapse into LA during ventricular systole these leaflets may not fit together causing blood to leak back into LA causing mitral regurgitation
57
regulation of normal blood pressure is dependent upon which systems
cardiovascular, necrologic, renal and endocrine systems
58
excessive vasoconstriction of the small arterioles
HTN this causes: increased diastolic BP, forces heart to create increased force of systolic pressure to get over after load excessive RAAS activation (=vasoconstriction)
59
cardiac effects of HTN
increased peripheral resistance --\> higher workload of heart --\> **cardiac wall hypertrophy** increased O2 demand and **stiff, non complaint ventricle** that doesn't relax --\> first heart failure and with time, systolic heart failure
60
vascular effects of HTN
increased **pressure on walls** of arteries --\> premature **wearing out of vessels**, accelerating atherosclerosis causes injury to arterials --\> arterial **walls weakened** and may rupture --\> resulting **hemorrhage**
61
renal effects of HTN
constricted renal arterioles --\> **decrease blood supply** to kidneys --\> **activates RAAS** increasing BP --\> increased glomerular after pressure result input and **degenerative changes in glomeruli tubules** --\> CKD
62
primary hypertension
unknown cause 90% of HTN
63
secondary hypertension
from unknown dx, potentially treated and potentially curable etiologies or secondary HTN: polycystic kidney disease, renal after stenosis, coarctation of aorta endocrine causes (hyperthyroid, pituitary or adrenal tumors)
64
atherogenic
creates athero-plaques trans fat and saturated fat
65
cholesterol
synthesized in body and from diet high levels are associteaed with premature atherosclerosis and increased CVD risk, transported by lipoproteins
66
lipoproteins
two types LDL and HDL
67
LDL
low density lipoprotein bad cholesterol carries cholesterol to the arteries
68
HDL
high density lipoprotein good cholesterol protective increases with regular excessive stoping smoking and modest alcohol intake carries cholesterol to the liver for removal
69
which medications cause drug included arrhythmias and infarcts
cocaine and methamphetamine intensifies effects of sympathetic nervous system
70
effects of cocaine and meth on heart
i**ncreases heart rate** (increased oxygen demand), **muscle irritability** (presdisposed to arrhythmia), **peripheral vasoconstriction , and coronary artery spasm, fatal arrhythmias and MIs**
71
main risk factors for CAD
cigarette smoking diabetes CKD elevated blood lipids high BP
72
secondary risk factors for CAD
obesity and type A personality
73
complications of MI
1. arrhythmia 2. heart failure 3. intracardial thrombi 4. pericarditis 5. cardiac rupture 6. papillary muscle dysfunction 7. ventricular aneurysm
74
beta 1 adrenergic receptors
common in heart and mediate isotropy and chronotropy minimal vasoconstiction
75
beta 2 adrenergic receptors
blood vessels induces vasodilation adronergic chronotrophy ionotrophy
76
adronergic
sympathetic nervous system effect beta 2 receptors
77
chronotropy
heart rate beta 2 receptors
78
inotropy
strength of heart contraction beta 2 receptors
79
dopamine receptors
present in renal splanchnic (mesenteric), coronary, and cerebral vascular beds
80
Describe why a small pulmonary embolus is more likely to cause a pulmonary infarction
With a large emboli it is going to **get caught in a main bronchus but it will have collateral blood flow** so that is why they aren't likely to cause infarction
With a small emboli, there is **less likely to be collateral circulation** to little alveoli in the depths of the lungs so its more likely to cause in infarction
KCSU17 Patho/Pharm Submodule 2
flashcards
Decks in class (14)
# Cards
-
Renal Physiology69
-
Tips3
-
Urologic and Renal Disorders85
-
Cardio Objectives80
-
Pulmonary Disease Objectives76
-
Pulmonary Disease Medications23
-
Cardio Pharm -- MI24
-
Cardio Pharm -- Arrhythmia22
-
Cardio Pharm - Heart Failure36
-
Cardio Pharm- HTN26
-
CardioPharm Vascular Disorders7
-
Cardio-Pharm Shock6
-
GI116
-
GI 6/12/1787
