1
Q
What are the characteristics of deep vein thrombosis?
A
- immobility and vasocongestion
- lower extremity fracture
- onset of calf pain
- history of cancer/long term surgery
- 3mo after surgery
-
2
Q
What does the endocrine system do?
A
- synthesize and release hormones transported to cells/organs through the blood stream
- the nervous system and endocrine system are connected
3
Q
How does the endocrine system develop?
A
- it stems off (differenciates) from the reporductive and central nervous systems in a fetus
- system stimulates gorwht and development in childhood and adolescence
- declines as people age since linked to male and female reproductive systems
- help maintains homeostatis
- initiats corrective and adaptive responses when emergency demands occur
4
Q
What hormones does the Anterior pituitary gland secrete?
A
stimulating hormones - released so that more hormone is released
1. thyrotropin (TSH)
2. adrenocorticotropin (ACTH)
3. follicle stimulating hormone (FSH)
4. Lutenizing hormone (LH)
Effector hormones - directly reacts to target tissue
1. Growth hormone (GH)
2. prolactin
5
Q
What hormones does the posterior pituitary gland secrete?
A
- antidiuretic hormone (ADH)
- oxytocin
6
Q
When does pathology occur?
A
dysfunction of releasing tropic or effector hormones or when defects occur in target organs
- either primary or secoundary
7
Q
What disease is eptopic hormone production?
A
paraneoplastic syndrom
- looks like cusing sydrom
8
Q
What is ectopic hormone production?
A
production of hormone or hormone-like substance from another source
9
Q
How does the neuroendocrine respond to stress?
A
- adrenal gland (medulla) releases catecholamines into blood (epinephrine, norepinephrine, dopamine)
- cortisol is also released to regulate metabolism, as a source of energy and protein syntheis, to dampen inflammatory response and to modulate perceptual and emotion functioning
- endorphins modulate pain perception
- growth hormone increases during acute stress but decreases during chronic stress
10
Q
What are musculoskeletal signs and symptons of endocrine disease?
A
- rheumatoid arthritis
- proximal muscle weakness
- perpeutates tender/trigger points
- carpal tunnel syndrome (could be caused by diabetes or pregnancy, usually bilateral and hands stiff from tenosynovitis)
- Periarthritis and calcific tendinitis (in shoulders)
- chrondrocalcinosis due to pseudogaut-calcium salts in joint cartilage, hyperthryroidism, hyperparathyroidism, acromegaly, and shoulder impingement
- spondyloarthropathy (spine pain and stiffness) - hemachromatosis, acromegaly, and diabeties
11
Q
What is cushing’s disease?
A
excessive levels of cortisol hormone caused by a tumor in the pituitary gland that causes the gland to produce too much ACTH
12
Q
What is cushing’s syndrome?
A
excessive levels of cortisol hormone due to causes outside of the body that increase the levels of cortisol, such as taking medications containing cortisol (corticosteriods)
- could cause tumor somewhere else
13
Q
What is the anterior pituitary lobe gland disorder?
A
- caused by tumors, pituitary infarction, genetic disorders, and trauma
- leads to hyperpitutiarism (oversecretion of hormone)
– crushing’s disease: leads to abnormal growth patterns, anemorrhea (lack of cycle), glactorrhea, gynecomastia, and impotence in men
— locally it can lead to visual field abnormalities, headaches and sleepiness
14
Q
What can crushing’s syndrome lead to?
A
- caused by not taking all corticosteriods perscribed, or by oversecretion of adrenal gland by lung cancer
- causes hyperglycemia (type 2 diabites due to abnormal fat), hypertension, proximal muscle wasting and osteoporosis (brittle bone disease)
15
Q
What does GH secreting ademoas do?
pitutiary gland disorders anterior lobe
A
produce cartilaginous and connective tissue overgrowth
16
Q
what is gigantism?
pituitary gland disorders: anterior lobe
A
-overgrowth of the long bones
develops abruptly in children before the epiphyses of the bone close
know differene between giagantism and acromegaly
17
Q
What is acromegaly?
pituitary gland disorders: anterior lobe
A
- increased bone thickening and hypertrophy of soft tissues
- develops slowly after the closure of epiphyses (devlops in 20/30 yr olds)
- affects face, jaw, hands and feet,
- local manifestations of headache, diplopia (sees double), blindness, lethargy
- muscle weakness and joint mobility issues
know difference between acromegaly and giagantism
18
Q
What is hypopituitarism?
pituitary gland disorders: anterior lobe
A
- rare
- caused by removal or destruction of the pituitary, pituitary tumors, postpartum hemorrhage, or reversible functional disorders
- clinically manifestations depend on age but include: growth hormone deficiency, adrenocortical insufficiency (low blood sugar and hypotension), hypothyroidism, gonadal failure/infertility, and visual impariments/neurological signs
19
Q
What is diabetes insipidus?
pituitary gland disorders: posterior lobe
A
- physiological impalance of water and ADH due to injury/loss of hypothalamus/posteriory pituitary gland
- excretion of large amount of urine (but no sugar in it)
- dehydration
fatigue/irritability - can be treated w/ADH pills
20
Q
What is Syndrome of inappropriate antidiuretic hormone secretion (SIADH)?
pituitary gland disorder: posterior lobe
A
- excessive release of ADH which disturbs fluid and electrolyte balance, resulting in water imbalance
- hyponatremia (decrease in sodium) and water intoxication occur as a result of fluid retention
- causes: tumors, infection, trauma
- CNS dysfunction
21
Q
What is hyperthyroidism?
A
- excessive secretion of thyroid hormone
- most common form is** grave’s disease** which increases T4 production
- Sjogren syndrome (dry eyes/mouth from dry membrane) and rheumatoid arthritis are at increased risk of graves disease
- thyroid stimulating immunoglobulins (TSI react against thyroglobulin which results causes T-4 to stop being suppressed
- stimmulates symmetrical enlargement of thyroid cell membrane and increases sympathetic nervous system activty through increasing the number of beta-adrenergic receptors and increasing the secretion of catecholamines
22
Q
What is a goiter?
A
- an enlargement of the thyroid gland
- can happen due to lack of iodine, inflammation or tumors
- causes a pressure on the trachea and esophagus which causes difficulty breathing, swallowign and hoarseness
23
Q
what are clinical manifestations of hyperthyroidism?
A
- CNS effects: tremors, irritability, increased deep tendon reflexes
- Cardiovascular and pulmonary effects: increased RR, HR, CO; arrythmia- musculoskeletal: weakness and atrophy
- integumentary: increased hair loss, heat intolerance
- ocular: exophthalmos (bulging eyes), sensitivity to light
- gastrointestional: weight loss, increased bowel movements, dysphagia
- Genitourinary: polyuria, infertility
24
Q
What is hypothyroidism?
A
definiency of thyroid hormone that results in generalized slowed metabolism
- type 1 primary: reduced function of thyroid tissue
- type 2 secoundary: inadequate stimulation due to pituitary or hypothalamic disease
25
What is type 1 hypothyroidism?
- decrease in thyroid hormone, TSH increased from ant. pituitary gland
- does not respond fully to TSH so decrease in T3 and T4 to the body
- causes: congenital autoimmune thyroiditis, thyroid ablation, or medications
26
what is Type 2 hypothyroidism?
- failure of the pituitary gland to synthesize and release adequate amounts of TSH
- causes: tumor, pituitary insufficiency, sheehan's shydrome ( excessive bleeding during pregnancy)
27
What are some clinical manifestations of hypothyroidism?
- **CNS:** Slowed speech, fatigue, slow mental function, anxiety
- **musculoskeletal:** proximal muscle weakness, myalgias, carpal tunnel syndrome, back pain, decreased bone formation and resorption
**- cardiovascular**: bradycardia, severe atherosclerosis, hyperlipidemia, HTN
- **hematologic**: anemia, easy bruising
- **respiratory:** dyspnea, respiratory/muscle weakness
- **integumentary:** poor wound healing, thin brittle nails, dry'scaly skin
- **gastrointestinal:** weight gain, constipation, delayed glucose uptake
- **Genitourinary:** infertiility
**decreased metabolism**
28
What is thyroiditis?
- inflammation of the thyroid
- associated w/ hypo and hyperthyroidism
- some variations form pus (acute suppurative) or cause excess granulation tissue (acute granulomatous), but most are lymphcytic/chronic (hashimoto's disease)
- hashimoto disease: decrease in T2 and T4 (important for metabolism) and increased TSH, size of goiter will decrease w/treatment, is sitruction of the thyroid gland by lymphocytes and anti-thyroid antibodies = autoimmune disease
29
What are causes and symptoms of thyroid cancer?
- makes up 90% of all endocrine cancers
- caused by history of radation to head, neck or chest
- red flags: vocal cord paralysis, ipsilateral cervical lympadenopathy (enlarged lymph nodes), hard painless nodules
30
What is a tyroid function test and what is it looking for?
- function: to diagnose or monitor pt w/ typroid disease
- screens for changes in thyroid hormone levels that directly effect metabolic function and muscle strength
- **important markers: thyroid stimulating hormone, T3, T4**
31
Why is thyroid stimulating hormone an important marker for tyroid function test?
because TSH differentiates between primary (associated w/ thyroid gland) and secoundary (associated w/hypothalamus and pituitary)
32
Why is T4 an important marker for tyroid function test?
**free T4: more accurate for measure thyroid function**
-TSh is produced by pituitary gland and signals for tyorid to produce T3 and T4, as it becans to circle the blood stream (metabolic rate) TSH production slows
33
WHat are TSH and T4 levels like for hyperthyroidism?
Low TSH but high T4
34
What are TSh and T4 levels like with primary hypothyroidism?
High TSH
low T4
35
What are TSH and T4 levels like for secoundary hypothyroidism?
low TSH and T4
36
What is T3 used to measure in the thyroid function test?
measurement used to diagnose hyperthyroidism
37
What are clinical implications for hypothyroidism?
- monitor for signs of hyperthyroidism if patient is on thyroid replacement therapy
- asses integumentary system for edema, skin lesions and wounds
- provide fall prevention screen as tyroid replacement therapy may increase risk for osteoporosis (bone fracture)
- assess for multisystem imparments as hypometablic state may result in elevate BP, respiratory impairment, weakness, myalgia, cold interolerance, poor glycemia controal and weight gain
38
What are the clinical implications of hyperthyroidism?
- monitor cardiac rhythm due to increased risk for atrial fibrillation
- monitor for symptoms of palpitations and nervousness
- educate patients to avoid exerise in hot settings, including outdoors and indoor pools
- assess for multisystem impairments as a hypermetabolic state may result in dysrtythmia, hypotension, weakness, muscle atrophy, unintentional weight loss
38
What kind of exercise should be done for hypothroid disease?
strength training/weight bearing to decrease the chance of bone fractures (osteoporosis)
39
What drugs are used for hypothyroidism/thyroid replacement hormone?
**- levothyroxine (T4)**
- liothyronine (t3)
40
What drugs are used for hyperthyroidism/anti-thyroid?
**- iodine**
- thiamines: propylthiouracil
**- propranolol (beta blocker)**
-- beta blockers increase hr which increases arhythmia, causes HR to not go up, use rate of percieved exertion not 220=age
41
What is hyperparathyroidism?
- overactivity of one or more of the 4 parathyroid glands
- disrupts calcium, phosphate and bone metabolism by making extra of them
- women more then men, often overlooked, caused by: aging, depression anxieity
-classified by primary, secoundary and teritary
42
What are the clinical manifestations of hyperparathyroidism?
- Early CNS symptoms: lethargy, poor memory, paresthesia, glove/stocking sensory loss, hyperactive deep tendon relfexes
- musculoskeletal: proximal muscle weakness, gout, muscle atropy, arthralgias
- Gastrointestinal: peptic ulcers, pancreatitis
- genitourinary: hypercalcemia, kidney infection
some people may be asymptomatic w// elevated serum and PTH levels
43
What is hypoparathyroidism and what causes it?
- hyposection, hypofunction or insufficient secretion of PTH (parathyroid hormone); bone resorption and GI tract absorption slow, serum ca levels fall and severe neuromuscular irritibilty develops -> serum phosphate levels rise when Ca falls
- causes: accidental removal of parathyroid glands, infarction due to inadepquate blood supply due to surgery, strangulation, scar tissue, hemochromatosis (iron build up), sarcoidosis (chronic inflammation), amyloidosis (protein build up), tuberclulosis (pulmony system disease), neoplasms, trauma or from an autoinnume disease
44
What are clinical manifestations of hyopoarathyroidism?
mild my be asymptomatic
neuromuscular irritabilty resulting in tetany
- acute tingling of fintertips, mout and feet: **trousseau's sign, chvostek's sign**
pseudophypoparathyroidism
- genetically associated w/shortened metatarsals and metacarpals
systemic manifestations: cardiac arrhythmias, intercostal muscle spasm
45
What is addison's disease: primary adrenal insufficiency?
- rare but can occur at anytime
- cause: idiopathic or autoimmune, medications, adrenal hemorrhage, radiation to adrenal galnds, kidney neoplasm
- risk factors: surgery, pregnancy, tauma, infection, salt loss from excess sweating (profuse diaphoresis), failure to stake steroids
**decreased production of cortisol**
- failure to inhibit anterior pituitary secrtion of ACTH
- increase in skin and mucous membrane migmentation
- widespread metabolic disturbances, hypoglycemia and liver glycogen deficiency, diminished resistance to stress (incr. infection), fatigue, hypotensive, weight loss, nausea, and vomiting, depression
**decreased production of aldosterone**
- fluid and electrolyte imbalance: increased sodium excretion, dehydration, hypotension, decreased cardiac outut, excessive K retention can result in arrhymia
- decreased tolerance of stress, poor coordination, fasting hypoglycemia
acute symptoms can include severe abdominal pain, low back or leg pain, severe vomiting, hypotension
46
what is secoundary adrenal insufficiency of addison's disease?
- adrenal gland still intact: aldosterone normal, deficiency in ACTH causing decreased cortisol
- caused by conditons outside adrenals: hypothalamic or pituitary tumors, removal of pituitary, rapid withdrawl of coritocsteroids (acute adrenal insufficiency)
- cause arthalgias, myalagias, tendon calcificaltion
- treatment: replace ACTH and monitor for fluid and electrolyte imbalance
47
What is diabetes and what are the two types?
chronic systemic disorder characterized by hyperglycemia and disruption of metabolism of carbohydrates, fats, proteins
- type 1: cannot produce insulin
- type 2L can produce insulin but body is resistant to it
48
What are the features of type 1 diabetes?
-diagnosed before 20; 10% of all cases; aprupt onset; viral, autoimmune, destruction of islet cells; genetic; have insulin antibodies; obesity uncommon;insulin production decreased, ketoacidosis may occur; treat with insulin, diet and exercise
- risk factor: first degree relative
49
What are the features of type 2 diabeties?
diagnosed before 40; 90% of all cases; gradual onset; obesity associated; no genetic association; no insulin antibodies; 80% obese; insulin production is variable and can be both above and below normal range; ketoacidosis is rare; treated through diet, oral hypoglycemic agents, exercise, and weight control
Risk factors: ethnic origin, hypertension, cigarette smoking, previous history, HDL cholesterol
**Long term type 2 diabetes leads to neuropathy and kidney disease**
50
What is the presentaiton of hypoglycemia?
**perspiration, weakness, pallor, nervousness, seizure, lethargy, irritability, tachycardia, headache**
Causes: excess insulin, hypothroidism, malnutrition, alcoholism
51
What actions should be taken with downward trendign hypoglycemia?
- consult w/ interprofessional if <100 mg/dL: ingest 15-30 g of fast acting carboydrate
- monitor blood glucose before, during and after exercise, monitor for cognitive impairment, may need to consider less stringent goals
**- someone w/ addican's disease might have hypoglycemia so need 15-30g of carbs**
52
What is the criteria for definding prediabetes for fasting plasma glucose and HbA1c?
- fasting plasma: 100 to 125 mg/dL
- HBA1c: 5.7-6.4%
53
What is glycosylated hemo9globin (HBA1c)?
- reflects mean plasma glucose concentration over previous 2-3 mo
- decreases w/ aerobic and strength training especially when both are done
- 1% decrease in HbA1c associated w/ decrease in major cardiovascular events and microvascular complications
- healthy older adults have a HBA1c below 7-7.5%, older adults with multiple issues have one from (8-8.5%)
54
What is the criteria for diabetes for fasting plasma glucose and AIC?
Fasting plasma glucose: less than or equal to 126
AIC: greater than or equal to 6.5%
55
What is the presentation, causes, and clinical implications of upward trending hyperglycemia?
presentation: polyuria (increased urination), polydipsia (drinking more water), blurred vision, weakiness, fatigue, dizziness; type 2 often asymptomatic
causes: diabetes mellitus, acute stress response, chronic kidney disease, acute pancreatitis, cushign syndrome
clinical implications: assess integumentary system, assess balance and fall risk, education regarding lifestyle modification, **no exercise if >250mg/dL w/ketones in urine**
56
What are microvascular and macrovascular complications of diabeties?
microvascular: blindness, kidney/renal disease, numbness and tinngling
macrovascular: stroke, cardiovascular disease, lack of blood flow in legs, slow healing wounds
57
What is a lipid profile?
-good indicator for overall health
- identifies risk for cardiovascular disease: cholesterol, triglyceride, lipoprotein
- abnormal levels lead to syslipidemia (elevated plasma cholester and/or triglyceride or low HDL
58
What is high density lipoprotein (HDL)?
helps to remove excess cholesterol deposits from the arterial lining
**- higher levels can reduce cardiovascular disease (>60 mg/dL)
- <35 mg/dL increase risk of cardiovascular disease - can be reversed if educate regarding lifestyle modification to promote healthy, wellness and movement**
---n
59
What are low density lipoproteins (LDL)?
**LDL deposits in blood vessels create plaque and occlusions, compromise circulation, and increase risk for atherosclerotic cardiovascular disease
- optimal: <100**
60
what are the causes, presentation, and clinical implications for upward trending LDL?
- causes: familial hypothroidism, liver or kidney disease, multiple myeloma
- lipid deposits on blood vessels, skin, eye, or tendons
- clinical implications: monitor for cardiovascular disease and neurodegenerative disease (alxheimers), educate for lifestyle modifications, assess integumentary system
61
What are triglycerides?
- Look at w/ LDL's to make sure fatty lipids transported approximently
- Assesses the body's ability to metabolize fat and recognize cardiovascular disease risk
62
What are causes, presentation, and clinical implications of Triglyceride?
- causes: glycogen storage diseases, hypothyroidism, diet high in carbodydrates and or alcohol, pregnancy, myocardial infarction
presentation: lipid deposits on blood vessels, skin, eyes or tendons paresthesia
clinical implications: consider refferal to other providers due to risk for multisystem presentations, monitor for vital signs, assess integumentary system, assess and monitor for cognitive impairment due to increased risk
| triglycerides tend to follow LDL trends
63
What is total cholesterol and what are optimal levels?
- main lipid associated w/cardiovascular disease
-assesses cardiovascular risk
- adult optiam low CVD risk: <140
- adult total cholesteral/HDL ratio: reccomended: >5:1, optimal: >3:1
64
What are the causes, presentation, and clinical implications of upward trending total cholesterol?
-causes: familial hypothyroidism, diet high in carbs and/or alcohol, hypertension, diabetes, pregnancy, myocardial infarction
-presentation: lipid deposits on blood vessels, skin, eyes, or tendons paresthesia
- clinical implications: monitor for cardiovascular disease, educate on lifestyle modifications, monitor for neurodegenerative disease (alzheimer's), assess integumentary system
65
What is glucagon?
- produced by pancreatic alpha cells
- increases blood glucose levels (energy utilization)
66
What is insulin?
- produced by bancreatic beta cells
- decreases blood glucose levels (energy storage)
67
What are the two steps in insulins pathway in glucose metabolism?
Step 1: insulin (signal) relased by beta cells = insulin secretion
Step 2: body cells detect and respond to insulin = insulin sensitivy (utilization or resistance)
68
What if the physiology of type 1 diabetes and how can it be fixed?
- dysfunction of step 1 (insulin secretion step)
- restore hormone level
- needs insulin: subcut injection or pumb, also beed basal (long/immmediate insulin for throughout the day and bolus for rapid short acting before a meal)
69
What is the physiology of type 2 diabeties and how can it be fixed?
- primarily dysfunction of step 2 (insulin sensitivity)
- antidiabetics manipulate hormone levelsL insuline stimulators increse insulin secretion, and insulin sensitizers decrease insulin reistance
70
Rapid acting insulin onset, peak and duration?
-i.e. insulin aspart
- onset: 15 min
- peak 45-90 min
- duration: 3-5 hrs
71
short acting insulin onset, peak and duration
- i.e. regular insulin
- 30min
- 2-3 hrs
- 3-8 hrs
72
What is an insulin pump and what are the advantages and disadvantages?
- external device that delivers insulin through catheter placed under the skin
- advantages: no needles
- disadvantages: still have to check blood sugar levels, cost, risk of malfunction
- **precautions: signs of hypo or hyperglycemia**
73
What are the two types of meds for type 2 diabetes?
**step 1: insulin stimulators - sulfonylureas: lowers blood glucose
- side effects: hypoglycemia
step 2: insulin sensitizers - biguanides: metformin (most common first line treatment for type 2 diabeties)**
- benefits: lowers blood glucose and AIC levels
- side effects: common/mild - GI system, nausea, vomiting, diarrhea; Rare: **lactic acidosis** (confusion, stupor, shallow rapid breathing, tachycardia)
74
How does exercise and diet impact diebeties?
- diet and exercise critical to effective diabeties management
- exercise: increase insulin sensitivity of peripheral tissues, weight loss = decr. body mass and drug requirements
- precautions: monitor for signs of hypo/hyperglycemia, check blood sugars, have carbs availible, schedule around meals/medication, don't inject into working muscle
75
What are the key concepts of the cardiovascular system?
* Cardiac output = HR x stroke volume
* blood pressure = cardiac output X total peripheral resistance
* rate-pressur eprduct (HR X SBP) represents the workload on the heart
* consider both forward and backward effects of impariment
76
What are the signs and symptoms of cardiovascular disease?
* chest pain/discomfort
* angina: chest pain from heart disease
* palpitations
* dyspnea
* cardiac syncope: lightheadedness
* vasovagal syncope
* cough
* cyanosis: blue/gray discoloration
* peripheral edema
77
What is atherosclerosis?
* disease that impacts coronary blood flow
* damage to inner layer of vessel walls w/blockages that protrude into the vessel
* coronary artery disase
* thickening of the arterial wall through accumulation of lipids, macrophages, T lymphocytes, smooth muscle cells, extracellular matrix, calcium and necrotic deris
*** pathology is the same for coronary artery disease, stroke, and peripheral vascular disase**
78
What is artheriosclerosis/small vessel disease?
uniform deposits around inner vessel walls, also called coronary micorvascular disease
79
What is the pathogenesis for atherosclerosis?
*** chronic inflammatory process:** LDL-C deposition
* ca deposits making walls stiffer
* injury to endothelial lining: decrease in nitric oxide production/sensitivity, platelet activation, lipid deposition
* thrombus formation: clot that blocks lumen/opening to blood vessels
80
What are the risk factors of atherosclerosis?
** modifiable:** smoking, elevated total serum cholesterol, elevated LDL-c, hypertension
** nonmodifiable:** age, family history, race/ethnicitgy, sex
81
What are the clinical manifestations of atherosclerosis?
* must have acritical deficit in blood supply to produce symptoms
* painand dysfunction: development of collateral circulation
* angina: chest pains
* shortness of breath
* palpitation
82
What is the difference between coronary artery disease and coronary microvascular disease
* clinical presentation: coronary artery disease has chest pain described aas crishing radiating to left arm, jaw, upper back and leads to cold sweat and nausea while coronary microvascular disase presents as diffuse discomfort, extreme fatigue, depression, dyspnea and in older adults - confusion
* pathology: CAD - plawue build up that extends in toward sthe blood vessel lumen; CMD: micorvascular constriction, plauque deposited uniformaly around inside of artery walls
* dianosis: CAR= Stress test, coronary angiography; CMD = sress testm functional vascular imaging
* treatment: CAD: surgery, medication; CMD: medication
83
What is the spectrum of ischemic heart disease?
* myocardial ischemia: situations where oxygen supply to heart muscle does not meet oxygen demand
* nstable angina: symptoms but not perdictible anymore
* acute MI: heart attack
* ishemic ardiomyopathy: vessel walls damaged
* heart failure
* death
84
What are the stages of angina pectoris?
* stable angina (exertional): cardiac workoad exceeds oxygen supply, resolves w/rest or nitroglycerin
* unstable or perinfraction: warning signs before heart attack, ER emergency
* New onset angina: go to ER right away, first time in last 2 weeks
* postinfarction: these symotoms right after Heart attack
* prinzmetal angina: spasm of corinary arteries, different cateogories, not very common
* Resting: reduced when sits up or stands
* micorvascular: lasts greater than 10-15min, small vessel disease
85
What is the pathogenesis behind angina pectoris?
imbalance between cardiac workload and oxygen supply to myocardial tissue
* decreased oxygen supply caused by vessels (spasm/atherosclerosis), circulatory factors (arrhythmias, aortic stenosis, hypotension), and blood factors (anemia, hypoxemia
increased oxygen demand (hyperthyroidism, exercise, emotion) yet doing more work
86
What is myocardial infarction and what are its risk factors?
development of ischemia with resultant necorsis of myocardial tissue: end result of angina that doesnt get resolved
* risk factors: smoking, cocaine, exertion-realted, aortic stenosis, Am time, seasonal , respiratory tract infections, silent ischemia
87
What are they symptoms of a myocardial infarction?
* sudden sensation of pressure radiating to arms, throat, neck
* pain constant lasting 30min to hours
* pallor, shortness of breath, profuse sweating
* catecholamine release results in cold and clammy, diaphoresis
*** women: unexplained fatigue, shortness of breath in middle of night**
* nausea and vomiting
* post infarction complications
88
How does the tissue of the heart change after a myocardinal infarction?
* 6-12 hrs: healing has not begun
* 18-24 hrs: inflammatory response, intraceullular enzyme release
* 2-4 days: visible necrosis (scaring), debris removal, recovering from anabolic state
* 4-10 days: debris cleared, collagen matrix laid down
* 10-14 days: feeling better but area vulnerable to stress, weak, fibrotic scar tissue with beginning revascularization
* 6 wks: scarring complete, tough, inelastic, unable to contract and relax like health tissue
89
What is the difference between type 1 and type 2 myocardial infarctions?
type 1: acute plaque rupture in 1 or more large coronary arteries, resulting in disruption of blood flow to section of heart muscle: heart attack
type 2: severe supply demand mismatch with inadepuate delivery of oxygenated blood to heart muscles more globily - more mild symptoms
90
What is orthostatic hypotension and what causes it?
decrease in 20mm Hg of systolic BP or 10 mm Hg drop in systolic and diastolic BP with an incrase in HR of 15 BPM
causes: dehydration, venous pooling, meidcations, immobility, malnutrition, valsalva, automic nervous system dysfunction (POTS)
90
what are clinical manifestations of orthostatic hypotension?
dizziness,blurry vision, synocope or fainting, palor, lethargy, weakness
older individuals: confusion, falls or mobility issues, cardiac symptoms
90
What is the pathogenesis of hypertension?
* regulated by two factors: blood flow (cardiac output), peripheral vascular resistance (increased resistance as a resut of narrowng of arterioles)
* symptoms: **very frequently asymptomatic**; may include headahces, vertigo, flushed face, blurred vision
91
What is heart failure and what can cause it?
complications of ischemic and hypertensive heart disease
* heart is unable to pumb sufficient blood supply the body needs
* due to disorders of the: cardiac valves, coronary arteries, myocardium, pericardium, large vessels
characterized by acute exacerbations of chronic conditions
92
What are compensatory mechanisms the body takes when heart failure starts to occur?
* ventricular dilation allows for more filling
* ventricular hypertrophy improves contractility
* sympathetic nervous system: increase HR and blood pressure through vasoconstriction
* renin-angiotension-aldosterone system: activated by baroreceptors to increase blood volume through retention of sodium and water
93
what are the long-term consequences of heart failure compensations?
* larger ventricular chamber
* thicker ventricule walls
* increased heart rate
* increased blood pressure
* increased fluid volume
---n
94
How is heart failure categorized?
based on how much it impacts someone's daily life
95
What is the difference between left sided vs. right sided heart failure?
left side: cateogirzed by reduction in ejection fraction, if the ejection fraction is reduced then its systlic heart failure but if preserved ejection fraction then diastolic heart failure
right sided: may be caused by left sided heart failure, valve disease or congenital heart disase; cor pulmonale: R heart failure that results from chronic pumlonary disase
96
What is cor pulmonale and what are its symptoms?
R heart failure due to COPD, PE or other pulmonary conditions
* vasoconstriction or obliteration of pulmonary vessels puts excessive stress on R ventricle
* symptoms: cardiac output drops w/exercise, exertional dyspnea, wheezing, fatigue, **distended neck veins, depended peripheral edema**
97
What are symptoms of right ventricular failure?
dependent edema, jugular venous distention, abdominal pain, weight gain, right upper quadrant pain, cardiac cirrhosis (ascites, jaundice), cyanosis, anerexia, nausea
98
what are symptoms of left sided heart failure?
progressive dyspnea, pulmonary edema, productive spasmodic cough with frothy sputum, cerebral hypoxia (confusion, irritability, impaired memory), fatigue and exercise intolerance, muscular weakness, renal changes
99
What is cardiomyopathy?
specific types of heart muscle dysfunction that results in heart failure
- inherited or acquired through genetic, mixed, postpartum, or chemotherapy induced
100
What is hypertrophic cardiomyopathy?
* genetically transmitted as an **autosomal** dominant trait
*** most common cause of sudden cardiac disease in young athletes**
* left ventricular hypertrophy, rigidity: decreased diastolic function, imparied ventricular filling
* dyspnea due to high pulmonary pressures
101
What is dilated cardiomyopathy?
* extensively damaged myocardium resulting in **enlargement**; heart ejects blood less efficiently
* risk factors: 50% idiopathic, obesity, smoking, long term alcohol use, infection
* non-specific symptoms like fatigue, weakness, chest pain, low or normal BP
102
What is restrictive cardiomyopathy?
* result of myocardial** fibrosis,** hypertrophy, infiltration, or defect in myocardial relaxation
* marked scarring of ventricles
* **rigidity** imparis diastolic blood filling
* clinical manifestations relate to decrased cardiac output, signs of CHF, exercise intolerance, fatigue, shortness of breath
103
What is pericarditis?
* inflammation of the pericardium: restriction in movement/function, pericardial effusion
* causes: idiopathic, infections, myocardial injury, chronic anemia
* presentation depends on etiology: pleuritic chest pain w. lying down, fever, joint pain, dyspnea, or difficulty swallowing
104
What is infective endocarditis?
* infection of the endocardium including valves: vegetations and streptococci/straphylococci
* risk factors: cardiac surgery, IV drug users, immunocompromised, degenerative heart disease, congenital
* initially have musculoskeletal symptoms of joint pain and myalgia
105
What is rheumatic fever and heart disease?
* form of endocarditis caused by streptococcal group A bacgeria
* scarring and deformity of heart valves
* inflammatory process in conenctive tissue: fever and joint pain, antigens to streptococcal cell bind to brain, heart, muscle and joints
* acute migratory polyarthritis
* dyspnea
106
What are three types of valvular disease?
* stenosis: narrowing or constriction that prevents the valves from opening fully: usually due to fibrosis, scarring, calcium deposits; incrased resistance to flow of blood
* insufficiency (regurgitation): valves do not close properly causing blood to flow back into the previous chamber
* prolapse: enlarged leaflets of AV valves bulge backwards into atrium
107
What is mitral stenosis?
* mitral valve thickened
* rise in left atrial pressure: causes R heart to fail
* murmer
* may be asymptomatic
* dyspnea and fatigue
* right sided heart failure
108
What is mitral regurgitation?
* mitral leaflets do not close properly so blood is ejected into both the left atrium and aorta
* progressive enlargement of left atrium: pulmonary congestion and hypertension
* causes: ischemic heart disease, rheumatic heart diase, collagen vascular disase, cardiomyopathy
* asymptomatic initally, then presents like left ventricular heart failure
* dyspnea
109
What is mitral valve prolapse?
* leaflets bulge backwards into L atrium
* varition in structure or shape of mitral valve
* commonly asymptomatic
* causes: marfan's syndrom, rheumatic fever, atherosclerosis, lupus, acromegaly, mitral valve prolapse syndrome
* only 1% have smptoms of profound fatigue, dyspnea and palpitations
110
What is aortic stenosis?
* progressive valvular calcification
* risk factors: obesity, sedentary lifestyle, smoking, high cholesteral
* outflow obstruction incrases pressure in left ventricle due to narrow opening: left ventriculr hypertrophy, elevated left atrial pressure, pulomary congestion
* dyspnea, exertional syncope
* high risk for sudden cardiac death
111
What is aortic insufficiency?
* leakage during diastolic: valve allows flow of aortic blood into left ventricle
* symptoms: exertional dyspnea, excessive perspiration w/exercise, paroxysmal nocturnal dyspnea, pulmonary edema
112
What are arrhythmias and what are their symptoms?
* disturbance of HR and rhythm, classified by origin
* symptoms: asymtomatic, fatigue, dyspnea, syncope, dizziness, diaphoresis, palpitations
113
What is an aneurysm?
* abnormal stretching (>50%) in the wall of an artery, vein or heart
* named for specific site of formation: seen in thoracic aortic and abdominal
* atherosclerosis erodes the vessel wall, formation of sac by stretching the inner and outer layers
* bulge w/ each systole
114
What are clinical manifestations of aneurysms?
* mainly asymptomatic
* vague substernal, back neck or jaw pain
* dysphagia, venous distention, dyspnea, mi and stroke with dissection of aortic arch
* abdominal aortic: rubture through all 3 tunica, bleeding into thorax/abdomen
115
How is the heart impacted in conective tissue diseases?
| lupus carditis, rheumatoid arthritis, ankylosing spondylitis, scleroderm
* lupus carditis: targets all parts of the heart - pericarditis, myocarditis
* rheumatoid arthritis: fibrinoid necrosis
* ankylosing spondylitis: aortic insufficiency
* scleroderma: sclerosis (hardening) of small arteries; HR or arrhythmias
116
what is congenital heart disease?
* anatomic defect in the heart that develops in utero during the first trimester
* cyanotic: **transportaion of the great vessels, tetralogy of fallot** (4 abnormal findings about heart in utero)
* acyanotic: **ventricular or aterial spetal defect**
117
arteriral vs. venous damages
* arterial: restrictions/blockages w/ blood flow and oxygen
* Venous: comes from venous circulation not moving fluid effectively back towards heawrt
* major difference is that arterial wounds are dry while venous wounds are wet
118
What causes an arterial occlusion and what does it result in?
**cause:** thrombus (atherosclerosis), embolism or trauma
**results in:** absent or decresased pulse, complete or partial loss of circulation to an extremity; may lead to tissue ischemia and gangrene if lack of collateral circulation
119
What factors effect decreased arterial flow on periphreal tissue?
* site of lesion
* severity of lesion
* metabolic demand of the tissue beyond the lesion
* extent of collateral circulation bypassing the lesion
120
What are signs and symptoms of arterial disease?
* changes in skin color and temperature
* pallor w/ elevation
* rubor (redness) of dependency: skin flushed and red temporalaly after bringing it down after being up
* shiny, waxy skin, decreased skin grwoth and temp
* dry skin
* ulcerations
* gangrene
* sensory disturbances, motor loss, pain: claudication - burning cramping
121
What is acute thrombophlebitis (thrombosis)?
an acute inflammatory condition with occlusion of a superficial or deep bein by a thrombus
122
What is the difference between superficial vs. deep acte thrombophlebitis?
* superficial: no generalized edema, inflammation along length of veins, redness, heat, tenderness, aching extremity (usually from IV)
* deep: generalized edema, painful and tender extremity; calf muscle tenderness incr. with ankle DF, systemic signs of inflammation, superficial veins may be distended, PE may be first sign
123
What are risk factors of venous thromboembolism (DVT)?
* prolonged immobility and bedrest
* age
* orthopedic injuries
* postoperative patients
* heart failure
* maligancy
* ues of oral hormal contraceptives
* pregnancy
prevention: avoid prolonged bedrest, early ambulation and exercise, thrombolytic boots/compression socks, avoid dehydration
124
What causes chronic venous insufficiency?
dependent edema, aching or tiredness in legs, increased pigmentaiton of the limb, sink ulceration and secoundary infection that can lead to cellulitis
125
What is vasculitis?
* involves blood vessels of any size, type or location
* affects PNS and CNS
* diagnosis through biopsy of symptomatic site and angiography
* treatmetn with corticosterios and immunosuppressive drugs
126
What is arteritis?
* most common form of vasculitis of the larg and med size vessels
* involves multiple sites of temporal or cranial arteries
* most common, increases with age
* usually sudden, sever, continuous unilateral headache with flu0like symptoms or visual disturbances
* treatment corticosteroids
127
What is thromboangiitis obliterans?
* an inflammatory reaction of the arteries to nicotine
* usually occurs in small arteries of the feet and hand and progress proximally
* results in decreased circulation to the extremities which may result in amputation
* improves if the person stops smoking
128
What are some vasomotor disorders?
raynaud's disease and complex regional pain syndrome
129
What is raynaud's disease?
* arterial disease caused by vasospasm
* usually affects arteries of the fingers
* caused by abnormality of the SNS
* usually occurs in young adults
* characterized by: senitivity to cold, blanching and cyanosis of the fingertips and nail beds, severe pain, sensory loss, numbness or tingling, decreased function of the hands
* symptoms relieved by warmth
130
What is hypoxemia?
decreased levels of oxygen in artrial blood
131
What is hypoxia?
decreased levels of oxygen in body tissue
| can be global and localized (raynouds disease)
132
What causes hypoxemia?
respiratory alterations: ventilation/perfusion mismatch, decreased oxygen in inspired air, hypoventilation, aveolar-capilary diffusion abnormality
cardiovascular compromise: pulmonary shunting
133
What are common signs and symptoms of respiratory disease?
* cough, dyspnea, chest pain, cyanosis, digital clubbing, abnormal sputum, altered breathing patterns
* refered in upper trap, shoulder, chest
134
What is pneumonia and what are possible risk factors?
* inflammatory response affecting the parenchyma of the lungs
* caused by bacterial, viral etc infections; inhalation of chemicals, smoking dust etc; aspiration of food, fluids etc.
135
What is the pathogenesis of pneumonia?
* aveolar macrophages cannot destroy pathogens: produce interleukins and tumor necorsis factor that damage the alveolar themselves
* microorganisms release damaging endotoxins
* air sacs and terminal bronchioles fill with infectious debris and exudate making it hard to breath
136
What are the clinical manifestations of pneumonia?
* sudden and sharp pleuritic chest pain
* hacking, productive cough
* dyspnea and tachypnea
* decreased chest excursion
* fever and chills
* headache, muscle pain
* fatigue
*** elderly: confusion and loss of balance** - walking pneumonia
137
What is pulmonary tuberculosis?
* infection of mycobacterium tuberculosis
* transmited by inhalation
* active Pulmonary tuberculosis has poor immunity, progressive primary TB, granulomas > caseous necrosis, spread to other parts of the body
* latent pulmonary tuberculosis: interact cells mediated immunity limit spread of organism, tubercles stay intact as long as immune system is intact but will still give a positive PPD test, not infectious and cannot be transmited
138
What are the risk factors of pulmonary tuberculosis?
* age
* immunocompromised
* end-stage renal disease
* economically disadvantated
* substance use disorder
* HIV
* diabetes
* residential facilities
139
What are the clinical manifestations of pulmonary tuberculosis?
asymptomatic in early stage, productive cough > 3 wks
weight loss
fever
abnormal breath sounds
tuberculosis meningitis
140
What is chronic obstructive pulmonary disease?
* chronic airflow limitation that is **irreversible**
* 2 kinds: chronic bronchitis and emphysema
* caused by exposure to environmental irritants like smoking and fuel combusion
* signs and symptoms: wheezing, weight loss, chronic dysnea, cough & sputum and chest tightness
141
What is chronic bronchitis?
* productive cough lasting for > 3mo/year for 2 consecutive years
* due to inflammatin and scarring of bronchial lining
* worse on expiration
* excessive mucus production
* symptoms: wheezing, cynosis, hypoxemia, cor pulmonale, frequent respiratory infections
142
What is emphysema?
* pathologic accumulation of air in lung tissue
* due to **loss of electicity **leading to prolonged respiratory problems and inflammation of upper long respiraotry ronchioles
* or **inherited deficiency of alpha 1 antitrypsin **which distroys the air space of alveoli, impacts lower lung fields
143
What are the clinical manifestations of emphsema?
* reduction of elastic recoil: dyspnea during phsical exertion, increased effort to exhale, usually no cough,
* alpha-1 antitrypsin deficiency: wheezing and dyspnea
144
What is asthma?
*** reversible** obstructive lung disease caused by inflammation and increased smooth muscle reaction of the airway to an irritiant
* chronic condition with acute exacerbations
* increased vascular permeability adn production of mucous
* mucous plugs
* impaired expiration eventually impairs inspiration
* clinically manifests through exhaustion, **nonproducive cough**
* may progress to irreversible changes and COPD
| extrinsic (responds to environment), intrinsic (body)
145
What is restrictive lung disease and what are the types?
* pulmonary conditino that reduces the lung volume and decreases compliance/total lung capacity: hard to breath in
* pulmonary fibrosis: chronic inflammation leads to scaring after active disease
* systemic sclerosis lung disease: autoimmune disease from excessive collagen deposition
* chest wall trauma: stab wound, broken rib etc.
146
What is pleurisy?
* a restrictive condition
* inflammation of the pleura
* wet (fluid increases abnormally) or dry (fluit content remains unchanged
* symptoms: **sudden sharp pain worse on inspiration**, cough, fever, chills
147
What is atelectasis?
* part of lung tissue collapses
* caused by obstgruction of bronchus, compression by air, blood or fluid
* symptoms: dyspnea, hypotension, cyanosis, increased temperature
* when lung function returns people need to breath deeply enough to espand alveoli before it turns into pneumonia
148
What is a pneumothorax?
accumulation of air or gas in the pleural cavity caused by a **defect in the visceral pleura or chest wall**
- air in chest wall that collapses the lung
- sympotms: dyspnea, hypotension, pleural chest pain, cesssation of normal respiratory movement and sound
149
What is a pleural effusion?
* collection of fluid in the pleural space: usually around lung bases since gravity pulls it down
* common with heart failure and lympathic obstrution caused by tumor, pneumonia etc
* symptos: dyspnea, nonspecific chest discomfort or pleuritic which is sharp and exacerbated by caughint
150
What is the pathogensis of lung cancer and risk factors?
* women more susceptible due to interaction btwn estrogen receptors and epidermal growth factor (women are also more susceptible to damage from smoking that causes COPD)
* sequence of genetic change is unknown
* risk factors: cigarette smoking, marijuna, environmental tonacco smoke, occupation esposure, previous lung disease (COPD, emphysema), nutrition, genetic susceptibility
151
How does lung cancer clinically manifest?
* ***cough*** is the most common presenting symptom
* dyspnea
* sputum production
* advanced: anorexia, fatigue, weight loss, bone pain, difficulty swallowing and hoarseness
152
what are the sympathetic receptors?
- Alpha 1: located in smooth muscle of arteries
- beta 1: located in heart
- Beta 2: located in lungs
153
Where/what are parasympathetic receptors?
* muscracarinic cholinergic receptors
* located in heart, and smooth muscles of airways
* decreases HR BP, contractility; constrict airway and increase resistance to air flow
154
How do cardiac/pulmonary medications interact?
* medication ment for lungs may impact heart and meducation for heart may impact lungs
155
What are bronchodilators?
expand airways
- beta-andrenergic (+) (sympathetic)
- anticholinergic (-) (parasympathetic)
156
What anti-inflammatories are used for cardiovascular and respiratory drugs and why?
* corticosteroids and luekotriene modifiers (block inflammation in long term management)
157
What are considerations for bronchodilators?
* long acting for control and short acting for acute problems
* administered by inhalation
* for those with asthma, COPD to decreases resistance of airflow and improve O2 and CO2
* may increase resting and exercising HR
158
What are bronchodilators: beta-androgenics used for?
* first line of treatment for asthma (short acting/rescue inhaler)
* terol: suffix, albuterol
* MOA: stimulates beta receptors
* inhaled
* side effects: bronchial irritaiton, increased HR stimulates CNS
159
What are bronchodilators: anticholinergics used for?
* often drug of choice for COPD management (not asthma)
* MOA: block parasympathetic cholinergic receptors
* usually ihaled
* side effects: constipation, urinary retention, tracycardia/increased HR
160
What are anti-inflammatory: glucocorticoids used for?
* chronic management of COPD and asthma
* MOA: inhibits prodction of proinflamatores, stimulates anti-inflammatory proteins
* admin: inhaled
* side effects: use lowest effective dose
* often combined with a long-acting beta-2 bronchodilator
161
what three systems are controlled for cardiovascular drug use?
SNS: alpha 1 and beta 1
PNS: vasodilated, decrease HR contractility
and renin-algiotension system: regulates blood pressure w/ fluid
162
How is hypertension treated?
*** first line of treatment is often a single drug:** diuretic, ACE inhibitor, beta blocker, calcium channel blocker
*** long term management often involves multiple medication
* depnds on patient and cormorbidities**
* usually oral
163
What do diuretic drugs do and what do they treat?
* reduce fluid volume by stimulating kidneys to increase urine output: lower blood volume = lower blood pressure
* side effects: dehydration and electrolyte imbalance
* PT impact: can lower resting and exercising BP, and lead to hypotension and orthostatic hypotention so need to monitor BP and HR and gradual cool down, hydrate and keep cool
164
What do ACE inhibitors treat and do and what do you need to keep in mind as a pt?
* captorpril, lisinopril
* block conversion of angiotension 1 to angiotension 2, and relax smooth muscles in artery walls (vasodilate
* suffix: pril
* uses: angina, hypertension, and heart failure
* side effects: cough and swelling of face/throat (angioedema) is rare, should not be used for those w/ kidney disease
* PT impact: NSAIDS may lower effectiveness of ACE inhibitors and increase risk of renal failure when combined, lower resting and exercise BP, risk of hyptension episode (less so than diuretics) so need to monitor BP and HR and ensure gradual cool-down
165
What do Beta-blockers treat and do and what do you need to keep in mind as a pt?
- block beta-adrenergic receptors which decreases HR and contractility
- suffix: olol
- used for hypertension and arrhythmias
- can be selective adn nonspecific so can lead to some degree of broncioconstriction
- side effects: bronchospasm in nonselective (bronchioconstriction), and orthostatic hypotension
- PT impact: **blunted/reduced HR response,** lower restin HR, hypotension so need to use other tests to measure fatigue, keep cool during exercise
166
What do calcium channel blockers treat and do and what do you need to keep in mind as a pt?
* limit calcium entry into vascular smooth muscle and cardiac muscle to cause vasodilation and slowed transmission of impulses between SA and AV node
* uses: HTN and arrhythmias
* suffix: dipine and pamil - nifedipine/verapamil
* side effects: fewer metabolic effects than other cardiac drugs, edema in feet/ankles, orthostatic hypotension, not indicated in systolic heart failure
* PT impact: orthostatic hypotension so monitor BP HR and rhythm
167
What do nitrates treat and do and what do you need to keep in mind as a pt?
* relax smooth muscle leading to vasodilation to better deliver oxygen blood
* used for cardiac ischemia dn angina (ex: nitroglycerin)
* oral, sublinual, IV, patch
* side effects: dizziness, headach, orthostatic hypotension
* PT impact: improves exercise performance, **have to have medication avaible to them as they exercise**
168
What do statins treat and do and what do you need to keep in mind as a pt?
* affect enzyme involved in producing cholesteral in liver: lowers cholesterol
* side effects: muscle pain/cramping, and headaches
* PT impact: increased risk for external rhabdomyolysis (muscle breakdown causing kidney damage) /muscle cramping so monitofr for signs of rhabdomyolysis and gradually increase exercise intensity
system based pathology
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