Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pathophysiology of chronic illness > final > Flashcards

final Flashcards

1
Q

hemostasis:
purpose?

A
  • stop blood flow from injured vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

role of thrombopoietin:

A

stimulates bone marrow to increase platelet (thrombocyte) production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

role of endothelium in hemostasis:

A
  • prevent and control blood clots
  • normally inhibits coagulation - prevents activated platelets from sticking to uninjured vessel walls
  • synthesizes von Willebrand factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

4 stages of hemostasis:

A
  1. vasoconstriction
  2. formation of platelet plug
  3. blood coagulation
  4. clot retraction and dissolution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

role of platelets

A

produced from megakaryocytes then break apart to form multiple platelets in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

role of vW (von Willebrand factor)

A

blood clotting factor = involved in platelet adhesion/ clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

vasoconstriction aka vessel spasm

A

decreases blood flow to injured vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

role of platelet plug formation:

A

platelets stick to endothelium at site of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

thromboxane A2 (TXA2)

A
  • stimulates activation of other platelets and platelet aggregation
  • produced by activated platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

role of blood coagulation:

A
  • coagulation cascades - stop bleeding out
  • intrinsic and extrinsic pathways, Ca+ involved in both
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

intrinsic pathway of blood coagulation:

A
  • activated by exposed collagen (endothelial injury in blood vessel)
  • longer and more complicated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

extrinsic pathway of blood coagulation:

A
  • activated by tissue factor ( released by endothelial cells due to platelet injury)
  • quicker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

role of clot retraction and dissolution

A
  • tissue heals
  • thrombin necessary - see definitions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

thrombin:

A

stimulates:
- formation of fibrin
- conversion of plasminogen to plasmin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

role of plasmin:

A

breaks down fibrin strands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

warfarins:

A

oral anticoagulants, block synthesis of prothrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

heparin:

A

blocks prothrombin activator
- prothrombin can’t be converted to thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

aspirin (ASA):

A

blocks platelet aggregation
- cant form insoluble fibrin clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

TPA aka thrombolytics

A

“clot-busters”
- prevent formation of insoluble fibrin clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

common indicators of blood clot disorders:

A
  • persistent nose/ gum bleeding or cuts bleed longer than normal
  • petechiae (tiny flat red spots on skin and mucous membrane)
  • easily bruised
  • blood in feces or vomit
    if untreated:
  • anemia
  • low BP, fast HR, faint
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

why mights platelet function be impaired?

A
  • inherited von Willebrand disease
  • over use of ASA’s, NSAIDS, warfarin
  • vitamin K deficiency, liver/ kidney disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

thrombocytopathia:

A

thrombus in a vein and accompanying inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

main risk factors for deep vein thrombosis - Virchow’s triad:
(risk factors)

A
  1. hyper-coagulable state (previous surgery, dehydration, cancer, pregnancy, obesity)
  2. venous stasis aka low blood flow over injury site (prolonged sedentary state)
  3. vessel injury (hypertension, bacteria, inflammation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

deep vein thrombosis
manifestations:
complications:

A
  • asymptomatic, then sudden or gradual aching and tenderness in area
  • hallmarks of local and systemic inflammation
  • maybe pain in calf when foot dorsiflexed

complications = thromboembolis (pulmonary embolism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

MAP =

A

cardiac output (Q) x total peripheral resistance (TPR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

hypertension aka HTN
- etiology
- pathogenesis
- treatment (diuretics only)

A

high BP = > 140/90mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

primary aka essential HTN:

A
  • chronic BP elevation w/o clear single identifiable cause -> due to arteriole vasoconstriction
  • increases work of heart and damage to endothelium in coronary, cerebral
  • 1 in 4 canadian adults
    risk factors: age, sex, genetics, ethnicity, diet, inactivity, smoking, kidney disease, stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

secondary HTN:

A

high BP due to another disease/ condition, commonly:
- renal disease
- adrenocortical disorders
- pheochromocytoma
- coarctation of the aorta
must treat underlying condition to manage BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

manifestations of uncontrolled hypertension:

A

early stages: asymptomatic, malaise, morning headache, fatigue
later: end organ damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

HTN treatment:

A
  • PA, diet
  • thiazide diuretics = increase fluid loss via urine, decreaing ECF and therefore venous return, and BP (reduce amount of NA+ and H2O in body by widening blood vessels)
  • ACE inhibitors = prevent body from producing angiotensin II (narrows blood vessels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

ARTERIOsclerosis:

A

all types of arterial changes:
- degeneration in small arteries and arterioles
- loss of elasticity
lumen gradually narrows and may become obstructed
- cause of increased BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

ATHEROsclerosis:

A
  • plaques consisting of lipids, calcium, and possible clots
  • related to diet, exercise, and stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

steps of lipid transportation:

A
  1. dietary intake of cholesterol and triglycerides
  2. chylomicrons absorbed into blood and lymph
  3. lipid uptake by adipose and skeletal muscle cells
  4. remnants to liver
  5. liver synthesizes lipoproteins
  6. LDL transports cholesterol to cells
  7. LDL attaches to LDL receptor in smooth muscle and endothelial tissue
  8. HDL transports cholesterol to liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

HDL composition

A

1/2 = protein
1/3 = phospholipid
<1/4 = cholesterol
<1/8 = triglyceride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

LDL composition

A

> 1/2 = cholesterol
<1/4 = protein
<1/4 = phospholipid
<1/8 = triglyceride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

primary hypercholesterolemia:

A
  • autosomal dominant disorder
  • mutation occurs in gene specifying LDL receptor in liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

secondary hypercholesterolmia

A

associated w lifestyle, obesity, diabetes, etc.
increased LDL production
suppressed LDL receptor synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what can an oxidized LDL do?

A

invade arterial wall, triggering inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

factors influencing oxidized LDL invading damaged endothelium and becoming a foam cell (early formation of an atherosclerotic plaque):

A
  • genetic predisposition to dyslipidemia, HTN, or diabetes
  • age, gender
    AND OR
  • dyslipidemia, smoking, hypertension, poorly controlled diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

progression of atherosclerosis (4):

A
  1. damage to endothelium
  2. development of fatty streak
  3. fibrous plaque
  4. complicated lesion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

step 1 - endothelium damage

A

can lead to:
- increased permeability
- leukocyte adhesion
- lipoprotein accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

step 2 - fatty streak development

A
  • mediators initiate smooth muscle cell recruitment and proliferation
  • accumulating LDL may get oxidized
  • LDL ingested by macrophages = foam cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

step 3 - fibrous plaque

A
  • continued SMC recruitment and proliferation
  • blood vessel lumen starrs to narrow
44
Q

step 4 - complicated lesion

A
  • as plaque grows the wall weakness and cell in core dies
  • plaque takes up space in vessel lumen
  • occlusion by thrombosis formation occurs if plaque ruptures
45
Q

peripheral vascular disease:
- manifestations
- treatment

A

= disease in arteries outside of heart usually due to atherosclerosis (often in femoral and iliac arteries)
manifestations:
- fatigue and weakness in legs
- intermittent claudication
- paresthesia in leg
- cool extremity and weak pulses distal to occlusion
treatment:
- medications to control risk factors
- increase collateral circulation by waking to point of claudication
- surgery

46
Q

angiogram

A

x ray test that uses special dye and camera

47
Q

auscultation

A

valvular abnormalities/ murmur

48
Q

cardiac catherterization

A

measures pressure and assess valve and heart function

49
Q

echocardiogram

A

records heart valve movements, blood flow, cardiac output

50
Q

electrocardiography

A

measures electrical activity of heart, used in initial diagnosis and monitoring of dysrhythmias, MI, infection, and pericarditis

51
Q

exercise stress tests

A

assess general cardiovascular function

52
Q

arrhythmias:

A

cardiac dysrhythmias = any disturbance/ variation in rate of cardiac muscle contractions/ heart conduction

53
Q

dysrhythmias w/ sinus node abnormalities:

A

bradycardia = regular sinus rhythm w/ HR <60bpm
tachycardia = regular sinus rhythm w/ HR>100bpm
might cause decreased CO

54
Q

dysrhythmias w/ atrial conduction abnormalities:

A

PACs = extra contraction/ ectopic beats
atrial fibrillation = rate >350bpm

may reduce CO, cause blood pooling in atria - increased risk of thrombus formation

55
Q

dysrhythmias w/ ventricular conduction abnormalities:

A
  1. bundle branch block = interference w/ conduction in one bundle branch
  2. PVC’s = extra beats from ventricular muscle cell or ectopic pacemaker (may lead to ventricular fibrillation)
  3. ventricular tachycardia = reduced diastole and likely reduce CO
  4. ventricular fibrillation = independent and rapid muscle fibre contraction - if not immediately treated = cardiac standstill
56
Q

what causes heart failure?

A

complication of other cardiopulmonary condition like:
- previous MI
- valve defect
- respiratory disease

57
Q

left sided heart failure - steps of manifestation (5):

A
  1. left ventricle weakens - can’t empty
  2. decreased CO to system
  3. decreased renal blood flow stimulates renin angiotensin and aldosterone secretion
  4. blood backup in pulmonary vein
  5. high pressure in pulmonary capillaries = pulmonary congestion of edema
58
Q

right sided heart failure - steps of manifestation (6):

A
  1. right ventricle weakens - can’t empty
  2. decreased CO to system
  3. decreased renal blood flow stimulates renin angiotensin and aldosterone secretion
  4. blood backup into systemic circulation = “venae cavae”
  5. increase venous pressure = edema in legs, liver, abdominal organs
  6. high venous pressure = distended neck vein, cerebral edema
59
Q

compensatory mechanisms in early stages of heart failure:

A
  • tachycardia
  • vasocontriction of skin arterioles
  • reduced urinary output
  • myocardial hypertrophy
60
Q

clinical manifestations of left vs right sided heart failure:

A

left = pulmonary congestion ex: orthopnea (breathlessness)
right =
- dependent edema
- distended veins
- cachexia and malnutrition
- swelling of liver or spleen

61
Q

aortic stenosis:
1. pathogenesis
2. manifestations
3. treatment

A
  1. normal aging/ congenital abnormalities in valve
    - calcification progresses from base to leaflets
  2. early = asymptomatic
    late = angina w/ exertion, dyspnea, syncope
    3.
    - reduce heart workload
    - prevent clots
    - may need to replace valve
62
Q

mitral stenosis:
1. pathogenesis
2. manifestations
3. treatment

A
  1. rhematic fever, aging, endocarditis
    - Calcification of mitral valve leaflets and chordae tendineae = impaired emptying of LA
    2.
    early = asymptomatic
    later = dyspnea, atrial fibrillation, rt-sided HF, cardiogenic shock
  2. same
63
Q

shock:

A

decrease in BP due to blood loss, loss of heart pump, or changes in TPR

64
Q

hypovolemic shock:

A

loss of circulating blood volume

65
Q

cardiogenic shock:

A

inability of heart to pump blood

66
Q

manifestions and progression of hypovolemic shock:

A

early = anxiety, thirsty
then=
- tachycardia
- cool, pale skin
- decreased urinary output
- continued thirst
- rapid respiration
eventually =
- lethargy, weakness
- metabolic acidosis
- decreased kidney function

67
Q

compensations to correct decreased BP:

A
  • increases SNS activity
  • increased renin-angiotensin - aldosterone activation
68
Q

complications of hypovolemic shock:

A
  • persisten vasoconstriction
  • stasis blood
  • damaged cells release cytokines - draw fluid into intersistial space
    eventually:
  • organ failure
  • respiratory distress syndrome
  • liver failure
  • ulcers
  • infection or septicemia
  • disseminated intravascular coagulation
  • depression of cardiac function
69
Q

cardiogenic shock:
etiology:
pathogenesis:
if untreated:

A
  1. MI, arrythmia, valve disease, cardiomyopathy
    2.
    - significant decrease in SV and CO even if HR compensates
    - such a drop in CO and result in drop in MAP
    3.
    - pulmonary congestion = dyspnea, pulmonary edema
    - systemic congestion = peripheral edema
    - insufficient organ perfusion = LOC, angina, decrease urine output)
70
Q

stable vs unstable plaques:
associated with =
fibrous caps =
block blood vessels?
form clot?
emobolus?

A

stable angina vs unstable angina and MIs
thick vs thin fibrous caps
stable = partially block vessel - dont form clots or emboli
unstable = plaque can rupture and result in clot occluding artery or becoming an embolus

71
Q

acute coronary syndromes:
list 3

A

when heart muscle suddenly becomes ischemic
- stable angina
- unstable angina
- MI
occur due to insufficient myocardial oxygen supply

72
Q

stable angina aka angina pectoris:

A
  • predictable and manageable
  • often a fixed stable plaque
73
Q

unstable angina:

A
  • unpredictable = increase frequency of symptoms that are sudden in onset/ severity
  • may be progression/ result of other conditions
  • often due to unstable plaque
74
Q

MI:
what is it?
how does it develop?

A
  1. atherosclerosis w/ thrombus attached = prolonged ischemia leading to cell death
    2.
    - thrombus obstructs coronary artery
    - vasospasm near plaque - obstruction
    - part of thrombus breaks away and blocks other coronary artery
75
Q

STEMI:

A
  • typically cull coronary artery blockage
  • ST segment elevation seen on ECG
76
Q

NSTEMI:

A
  • typically partial blockage of coronary artery
  • no ST segment elevation seen on ECG, other chnages and symptoms consistent w MI
77
Q

3 zones of tissue damage post MI

A
  1. area of necrosis =
  2. areas ischemia =
  3. area of injury/ inflammation =
78
Q

MI manifestations:

A

angina = severe crushing substernal pain or indigestion
anxiety/ fear
pallor
diaphoresis
nausea
dyspnea
hypo/hyper tension

79
Q

MI key diagnostic indicators:

A

blood tests:
- protein biomarkers
- CRP and WBC count
- electrolyte

  • monitor for hypoxemia
  • pulmonary artery pressure to asses ventricular function
80
Q

common MI complications:

A
  • sudden death
  • cardiogenic
  • arrhythmias
  • heart failure
81
Q

stents:

A

put in vessel, remove clot

82
Q

bypass:

A

diverts blood around narrowed/clogged parts of the major arteries to improve blood flow and oxygen supply to the heart.

83
Q

nitroglycerin

A

vasodilator

84
Q

beta blockers

A

slow HR by blocking beta-adrenergic receptors

85
Q

antiarrhythmics

A

slows conduction via AV node and increase contractivility

86
Q

Antihypertensive drugs

A

diuretics = increase excretion of water and Na+
ACE inhibitorus = block formation of angiostemm II and aldosterone

87
Q

anti-coagulants

A

ex: warfarin

88
Q

ASA

A

ex aspirin

89
Q

respiratory acidosis:
1. initiating event
2. result
3. compensation
4. manifestations
5. treatment

A
  1. impaired alveolar ventilation from other diseases
  2. increased PCO2 and drop in pH
  3. kidneys excrete more H, produce HCO3
  4. impaired NS function, leading to
    - headache
    - lethargy
    - weakness
    - confusion
    - coma
    - death
  5. improve ventilation
90
Q

metabolic acidosis:
1. initiating event
2. result
3. compensation
4. manifestations
5. treatment

A
  1. excessive drop in HCOS (diarrhea) or increase HCO3 buffering, renal failure
  2. decreased serum HCO3 and pH
  3. increased RR, H excretion, HCO3 production
  4. same
    • correct condition
    • restore fluids and electrolytes
    • supplemental sodium bicarbonate
91
Q

hypercapnia:

A

PaCO2 > 50mmHg
- large increase in CO2 lowers pH = respiratory acidosis

92
Q

hypoxemia:

A

PaO2 < 60 mmHg
- decrease in PO2 can lead to tissue ischemia

93
Q

hypoxia:

A
  • failure of oxygenation at level of tissue
  • not measure by lab tests
94
Q

general manifestations of respiratory disease:

A
  • sneezing, coughs, sputum, cyanosis
  • abnormal breathing
  • rales in lungs
    -dyspnea (breathing discomfort - shortness/ breathlessness)
95
Q

covid 19:
1. pathogenesis
2. staged responses

A

1.
- virus enters body via mucus
- has S protein to bind to ACE-2 receptors in cells
- use host cell ribosomes to makes new virus proteins
*most ACE-2 receptors are in lungs, blood vessels, kidneys, heart, CI tracts

2.
early = acute inflammation, cytokines released by infected cells, WBC’s recruited
later = continued cytokine release, coagulation factors activated, increased vascualr oermeability and edema

96
Q

covid manifestations

A

mild: fever, fatigue, cough, loss of taste/ smell, nausea/ diarrhea
moderate: worse dyspnea, tachypnea, hypoxemia, pulmonary edema
critical: respiratory failure, septic shock, organ dysfunction

97
Q

asthma:

A

reversible bronchial obstruction in peeps w hypersensitive airways, attackes can cause permanent lung damage and develop chronic asthma
*different kinds have same pathologic changes

98
Q

extrinsic asthma

A

acute type 1 hypersensitivity reaction

99
Q

intrinsic asthma

A

hyperresponsive airway as result of infection, stress, cold, inhaled irritants, exercise, some meds

100
Q

type 1 hypersensitivity reaction -
2 phases:

A
  1. immediate response:
    - inflammation, bronchoconstriction, edema, increased mucus secretion
  2. late phase reaction
    - ~2 hours laters
    - eosinophils amplify inflammatory reaction for 12-24 hours
101
Q

type 1 hypersensitivity reaction -
typical vs severe clinical manifestations:

A

typical:
respiratory alkalosis, cough, dyspnea, agitation, wheezing, phlegm, tachycardia, etc
severe:
respiratory acidosis, metabolic acidosis, hypoxia, continued other

102
Q

asthma treatments:

A

reduce exposure to allergens
controlled breathing techniques
brochodilator
glucocorticoids - reduce inflammation

103
Q

diabetes mellitus

A

metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion and/or insulin action

104
Q

type 1 a vs b

A

a = auto-immune attack on beta cells in pancreas causing an absolute insulin deficiency
b = same, but not due to autoimmunity

105
Q

3 p’s of hyperglycemia (in both types diabetes)

A
  • Polyuria
  • Polydipsia
  • Polyphagia
106
Q

type I diabetes manifestation

A

above + weight loss

pathophysiology of chronic illness (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions