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Pathophysiology > Exam1 ppt > Flashcards

Exam1 ppt Flashcards

1
Q

what is cardiovascular disease

A

altered oxygen/nutrient delivery and waste removal (too little) in tissues- usually hypoxia

affects other vascular tissues

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2
Q

components and functions of the CV system

A

heart=pump=high metabolic rate high O2 demand

vessels=conduit for blood=maintenance of BP

blood=carry O2 nutrients and wastes

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3
Q

potential heart problems

A

cant pump effectively or efficiently
mechanical issues, including electrical
areas of necrosis due to hypoxia

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4
Q

problems with vessels

A

increased pressure
decreased pressure
flow is affected
vessel wall injury

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5
Q

problems with blood

A

reduction in O2 or O2 carrying capacity
bleeding
clotting

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6
Q

what are causes of hypoxia

A

occlusions-> infarct (tissue necrosis)

inadequate ventricular filling or emptying

altered heart function

anemia

loss of blood volume (shock)

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7
Q

what structures monitor BP

A

carotid sinus and aortic arch baroreceptors
juxtaglomerular apparatus
receptors in walls of atria and large vessels

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8
Q

what mechanisms do BP receptors activate

A

neural: increase BP, decrease SNS stim leads to increased pressure in glomerulus which leads to increased filtration and increased urine output

RAAS
ANP
ADH

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9
Q

the body regulates fluid volume and composition both extracellularly and intracellularly by

A

regulating the volume and composition of blood

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10
Q

what is responsible for 90-95% of osmotic pressure

A

Na ions

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11
Q

how do electrolytes enter/exit the body

A

ingestion adds electrolytes to the body

kidney, liver, skin, lungs remove electrolytes from the body

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12
Q

what regulates osmotic pressure intracellulary

A

proteins

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13
Q

what is the primary control of osmolality

A

ADH is the primary hormonal control of osmolality

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14
Q

forces favoring filtration

A

capillary hydrostatic pressure (blood pressure)

interstitial oncotic pressure (water pulling)

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15
Q

forces favoring reabsorption

A

plasma oncotic pressure (water pulling)

interstitial hydrostatic pressure

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16
Q

what is edema

A

accumulation of fluid within the interstitial spaces

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17
Q

what are some causes of edema

A

increase in hydrostatic pressure

losses or diminished production of plasma albumin

increases in capillary permeability

lymph obstruction

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18
Q

clinical manifestations of edema

A

local: limited to site of trauma (cerebral, pulm, pleural effusion, pericardial effusion, ascites)

generalized: more systemic, dependent edema, LE swelling

increased distance for diffusion of O2 ( increased ECF= increased distance= decreased O2 diffusion)

decreased blood flow= poor wound healing

fluid is trapped/ not available for metabolism/ perfusion= dehydration (ex: shock/hypovolemia in burn patients)

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19
Q

what are some sodium balance effects on the brain

A

neurological function is altered (esp with hyponatremia)

rapid shrinking can cause tears in vessels/ hemorrhage

rapid swelling can cause brain herniation

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20
Q

what factors regulate Na retention

A

estrogens-mixed

glucocorticoids increase Na retention (cortisol binds to same receptor as aldosterone)

osmotic diuretics decrease Na retention

poorly reabsorbed anions decreased Na retention

diuretic drugs decrease Na retention

dopamine increases Na retention

drugs/toxin cause alter Na retention

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21
Q

what is the impact of K on body

A

influences resting membrane potential

linked to acid base balance

affects enzymes involved in carbohydrate metabolism and electron transport

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22
Q

how does increased aldosterone affect K regulation

A

-antiport effect with Na increased permeability of luminal membrane permeability to K

-allows tight control despite large increase in K intake

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23
Q

how does increased tubular flow rate affect K regulation

A

k diffuses across apical membrane into the lumen it follows that gradient, washing it down the tubule maintains the gradient necessary to keep it moving in the tubule

excess fluid loss decreases K in lumen

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24
Q

aldosterone disorders that affect synthesis of K regulation

A

addisons disease- deficiency of aldosterone

conns syndrome- excess aldosterone (primary aldosteronism)

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25
Q

effects of hyperkalemia

A

results from increased intake
renal failure
crush injuries

results in muscular weakness, irritability, vfib, ecg changes

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26
Q

effects of hypokalemia

A

results from excessive loss or decreased intake, kidney disease and certain diuretics

results in muscle fatigue, flaccid paralysis, mental confusion, increased urine output, ecg changes

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27
Q

where is majority of calcium stored

A

99% in bone
0.9% extracellular
0.1% intracellular

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28
Q

what does calcitonin do

A

stimulates osteocytes to deposit Ca within bone

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29
Q

what does PTH do

A

-bone reabsorption (osteoclasts)
-increase renal tubular reabsorption
-stimulates vitamin D
-increase intestinal absorption of Ca

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30
Q

how does acidosis affect Ca

A

acidosis frees Ca from proteins

increases in Ca reabsorption

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31
Q

how does alkalosis affect Ca

A

increases the % bound to proteins

pts more susceptible to tetany-relative hypocalcemia

decreases in Ca reabsorption

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32
Q

define hypercalcemia

A

Ca > normal
neuromuscular exciteability depressed
cardiac arrhythmia

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33
Q

describe hypocalcemia

A

ca < normal
nerve and muscle excitability
tetany

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34
Q

what ion affects resting membrane potential

A

K

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35
Q

what ion affects threshold

A

Ca

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36
Q

what causes metabolic acidosis with normal anion gap

A

diarrhea (most common)
renal tubular dysfunction (acidosis)
ammonium chloride ingestion
carbonic anhydrase inhibitors (CAI)

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37
Q

what causes increased anion gap with metabolic gap

A

methanol poisoning
uremia (renal failure=retention of acids)
lactic acidosis
ethylene glycol poisoning
pA-p-Aldehyde intoxication
ketoacidosis (DM, starvation)
salicylate poisoning

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38
Q

what is anemia

A

decrease in number of circulating RBCs or decrease in quality/quantity of hemoglobin

sign of another underlying problem

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39
Q

etiology of anemia

A

altered RBC production
blood loss
increased RBC destruction
combination of all 3

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40
Q

how are size of RBC classified

A

Identified by terms that end in “cytic”

macrocytic
microcytic
normocytic

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41
Q

how is hemoglobin content classified in anemia

A

identified by terms that end in “chromic”

normochromic and hypochromic

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42
Q

macrocytic normochromic anemia

A

B12 or folate deficiency

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43
Q

microcytic-hypochromic anemia

A

iron deficiency
thalassemia

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44
Q

normocytic-normochromic anemia

A

hemorrhage
hemolytic
aplastic

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45
Q

how does anemia manifest

A

hypoxia
fatigue
weakness
dyspnea
angina

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46
Q

how does the heart try to compensate for anemia

A

increase cardiac output by increasing the rate and strength of contraction

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47
Q
A
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48
Q

How can tissue hypoxia present

A

Ischemia
Weakness
Fatigue
Pallor
Increase RR
Dizziness/fainting

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49
Q

What are compensatory mechanisms for tissue hypoxia

A

Increased HR
Increase SV
Dilate capillaries
Increase renin aldosterone
Increase erythropoietin
Increase BPG cells

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50
Q

Pathological mechanisms of anemia of chronic disease

A

Decreased erythrocyte life span
Suppressed production of erythropoietin (kidney damage)
Ineffective bone marrow response to erythropoietin
Altered iron metabolism

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51
Q

What causes chronic disease anemia

A

Chronic disease or inflammation
Infections
Cancer
Autoimmune diseases

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52
Q

What is pancytopenia

A

Reduction of absence of all three types of blood cells
WBC RBC PLT

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53
Q

Pathophysiology of aplastic anemia

A

Hypocellular bone marrow that has been replaced with fat

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54
Q

What is aplastic anemia caused by

A

Pancytopenia results

Autoimmune disorders due to chemicals drugs physical agents unpredictable exposures, inherited or idiosyncratic cause

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55
Q

How does aplastic anemia manifest

A

Hypoxemia
Pallor
Weakness
Fever
Dyspnea
Signs of hemorrhaging if platelets affected

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56
Q

what is hemolytic anemia

A

accelerated destruction of RBCs
can be acquired or congenital

can be autoimmune or drug induced

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57
Q

describe autoimmune hemolytic anemia

A

autoantibodies against antigens normally on the surface of erythrocytes

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58
Q

describe drug induced hemolytic anemia

A

form of immune hemolytic anemia that is usually the result of an allergic reaction against foreign antigens

called hapten model

ex: PCN, cephalosporins (more than 90%) and hydrocortisone

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59
Q

what are clinical manifestations of hemolytic anemia

A

jaundice (icterus)
aplastic crisis (body not producing new RBC)
splenomegaly

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60
Q

what is hemostasis

A

formation of platelet plug
cascading reaction of many different clotting factors
vasoconstriction

strong connection between inflammation and clot formation

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61
Q

what are coagulation defects

A

vitamin C deficiency
hepatic failure
vitamin K deficiency
hemophilia
thrombocytopenia
factor V leiden mutation

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62
Q

describe vit C coag defect

A

causes problem in activating platelets
scurvy
lack of stable collagen-required in collagen synthesis

63
Q

describe hepatic failure coag effects

A

almost all clotting factors are made in the liver

64
Q

describe vit K coag defect

A

required to synthesize/modify prothrombin, and factors 7, 9, 10 protein C and S

helps clotting factors function more quickly and efficiently

allows clotting factors to interact with phospholipid surface

cause by fat malabsorption due to lack of bile secretion

65
Q

describe hemophilia coag defect

A

factor 8= hemophilia A (more common)
factor 9= hemophilia B
X linked chromosomal syndrome

66
Q

describe thrombocytopenia

A

bleeding small capillaries and blood vessels
low number of platelets
usually an autoimmune disorder

67
Q

describe factor V leiden mutation coag defect

A

common clotting disorder
mutation (R506Q) in the heavy chain of factor V; resistant to cleavage by APC
TFPI has a 2 fold decrease in inhibition
hypercoagulable state (most common genetic risk factor for thrombosis in caucasians

68
Q

pathological conditions of bleeding

A

platelet defects
clotting factor defects
vessel integrity
frank bleeding
inherited bleeding disorders (hemophilia A or B)

69
Q

pathological conditions of clotting

A

qualitative differences in platelet function

inherited coagulopathies (factor V leiden)

acquired hypercoagulability (protein S and C deficiency, antiphospholipid syndrome)

arterial thrombosis (atherosclerosis)

venous thrombosis (stasis)

CV abnormalities (afib)

vasculitis

70
Q

definition of thrombocytopenia

A

platelet count < 150,000mm3

<50,000-hemorrahage from minor trauma

<15,000- spontaneous bleeding

<10,000 severe bleeding

71
Q

causes of thrombocytopenia

A

hypersplenism
autoimmune
hypothermia
viral/bacterial infections that cause DIC
HIT

72
Q

what are the two types of thrombocytopenia

A

immune thrombocytopenia purpura

thrombotic thrombocytopenia purpura

73
Q

what is immune thrombocytopenic purpura (ITP)

A

IgG antibody that targets platelet glycoproteins

antibody coated platelets are sequestered and removed from circulation

the acute form of ITP often develops after a viral infections is one of most commonchildhood bleeding disorders

74
Q

how does immune thrombocytopenic purpura (ITP) manifest

A

petechia
purpura
major hemorrhage
bruising

75
Q

what is thrombotic thrombocytopenic purpura (TTP)

A

a thrombotic microangiopathy

dysfunction of the metalloproteinase ADAMTS13

platelets aggregate, form microthrombi, and cause occlusion of arterioles and capillaries

systemically platelet number is low

76
Q

what is essential (primary) thrombocythemia

A

platelet counts >600,000mm3

myeloproliferation disorder of platelet precursor cells
–megakaryocytes in the bone marrow are produced in excess

microvasculature thrombosis occurs

77
Q

what is a result of alterations of platelet function

A

increased bleeding time in the presence of a normal platelet count

78
Q

what causes platelet function disorders

A

platelet membrane glycoprotein and von Willebrand factor deficiencies

can be congenital or acquired

79
Q

how do platelet function disorders manifest

A

petechia
purpura
mucosal bleeding
gingival bleeding
spontaneous bleeding

80
Q

what is Virchows triad

A

endothelial injury (hypertension)

alterations in normal blood flow (atherosclerosis, vascular disorders, stasis)

hypercoagulability ( increased platelet function or increased clotting activity)

81
Q

what are issues associated with thrombosis

A

embolism
infarction
DIC

82
Q

what is DIC

A

Disseminated intravascular coagulation

complex acquired disorder in which clotting and hemorrhage occur virtually simultaneously

sudden onset of widespread thrombi in microcirculation with the rapid consumption of platelets and coagulation factors, fibrinolysis is activated, inability to contain thrombi

83
Q

what is a primary initiator of DIC

A

endothelial damage

84
Q

what is a result of DIC

A

death
ischemia
hypoperfusion

activating the fibrinolytic system (plasmin) the pts fibrin degradation product (FDP) and D dimer levels will increase which downregulates clotting

85
Q

what is treatment for DIC

A

fix the underlying cause

86
Q

clinical signs and symptoms of DIC

A

bleeding from venipuncture sites
bleeding from arterial lines
purpura
petechia
hematomas
symmetric cyanosis of the fingers and toes

87
Q

conditions associated with DIC

A

metastatic cancer
acute bacterial/viral infections
malaria (certain parasitic diseases)
sepsis
massive trauma
burns
amniotic embolism

88
Q

what is atherosclerosis

A

intimal lesions atheromas or fibrofatty plaques which protrude into and obstruct vascular lemns and weaken the underlying media

contributes 50% mortality in the western world

89
Q

where does atherosclerosis happen

A

higher pressure vessels/larger vessels often have it

bifurcations

chronic inflammatory problem

90
Q

what are the three principal components of atherosclerosis lesion

A

cells (macrophages/foam cells, smooth muscle cells, lymphocytes)

macrophages that are engulfed LDL

extracellular matrix (ECM/collagen)

lipid (LDL, oxidized LDL)

91
Q

factors that promote atherogenisis

A

endothelial injury that alters the normal hemostasis of the endothelium
–increased adhesion and permeability
–more procogulant
–formation of vasoactive cytokines and growth factors

continuing inflammatory response

cyclic accumulation of cells and lipids

92
Q

potential consequences of atherosclerosis

A

narrowing of vessels=ischemia

sudden vessel obstruction caused by plaque hemorrhage or rupture

thrombosis leading to embolism

aneurysmal dilation due to weakening of vessel wall (outside of the plaque)

93
Q

define hypertension

A

BP > 140/90

normal is <130/85

94
Q

pathogenesis of HTN

A

increased CO and or SVR
increases afterload
kidneys, RAAS, and SNS all contribute

95
Q

consequences of HTN

A

vessel injury
prolonged vasoconstriction-target organ disease
retinal changes
renal disease
cardiac disease (CAD, CHF)
neuro disease (stroke, dementia, encephalopathy)

96
Q

what are factors that lead to increased Na retention

A

-genetics
-increased SNS
-increased RAAS
-endothelial dysfunction
-dysfunction of natriuretic hormones
-renal glomerular and tubular –inflammation
-obesity
-insulin resistance
-increased dietary intake
-decreased dietary K, Mg, and Ca

97
Q

how does HTN manifest

A

injury to blood vessel wall
subsequent development of atherosclerosis
predisposition to all major athersclerotic CV disorders

left ventricular hypertrophy
is a risk factor for ischemic heart disease, arrhythmias, CHF, death

98
Q

describe ventricular remodeling

A

follows long term HTN, myocardial ischemia or MI

involves SNS and kidneys

results in vasoconstriction and hypertrophy of left ventricle

99
Q

what results from myocardial ischemia

A

coronary heart disease

100
Q

what typically precedes CAD

A

long period of progressive atherosclerosis

101
Q

when does CAD show symptoms

A

when it is fairly advanced because of the development of collateral circulation along with plaques

102
Q

what is the leading cause of death among males and females

A

CAD

103
Q

what is the pathogensis of heart disease

A

diminished coronary perfusion relative to cardiac demand

atherosclerotic narrowing of the coronary arteries (>75% occlusion in 90% of patients

the myocardial ischemia is precipitated by abrupt plaque changes followed by thrombosis and platelet aggregation

104
Q

what are the categories of heart disease

A

chronic ischemic heart disease
-stable angina (angina pectoris)

acute coronary syndromes
-unstable anginas
-MI

105
Q

what is a myocardial infarction

A

heart attack

death of cardiac muscle as a result of ischemia

106
Q

what is the leading cause of death in the US

A

MI

107
Q

what is the pathogenesis of MI

A

sudden change in plaque morphology

platelet aggregation and activation and thrombus formation

occlusion of vessel (minutes)

hypoxic injury and if prolonged, necrosis

108
Q

what is the difference between STEMI and NSTEMI

A

stemi has ST elevation on ecg (active infarction)

NSTEMI has st depression (ischemia)

109
Q

what are consequences of MI

A

loss of critical blood supply to myocardium which induces functional and biochemical consequences

hypoxic cell injury

cell death (necrosis) -> wound healing response

decreased function

arrhythmias

congestive heart failure

cardiogenic shock

110
Q

what is sudden death in CHD patients from

A

vfib

111
Q

how do arrhythmias occur

A

the ischemia seems to induce the cardiac muscle to become electrically unstable such that it fails to contract in a coordinated fashion and expel blood from the heart

likely due to dysregulation of ion balance across the cardiomyocyte membrane

112
Q

what are some disorders of the myocardium

A

called cardiomyopathies

dilated cardiomyopathy (congestive cardiomyopathy)

hypertrophic cardiomyopathy
-asymmetric septal hypertrophy
-hypertensive (valvular hypertrophic) cardiomyopathy

restrictive cardiomyopathy

113
Q

disorders of the endocardium

A

valve disorders
rheumatic heart disease following GAS infection
infective endocarditis (mainly bacterial), can be viral, fungal or paracytic

114
Q

what are the 3 hallmarks of endocarditis

A

endocardial damage
bacterial adherence
formation of vegetations

115
Q

what is the survival rate of heart failure

A

50%

116
Q

how many people in US have heart failure

A

4.8 million

117
Q

what are the two factors are involved in the pathophysiology of heart failure

A

-decrease in cardiac output
-decrease in perfusion to other organs (think kidneys)

compensatory mechanisms to maintain perfusion

118
Q

what are the hearts compensatory mechanisms

A

frank starling mechanism
increased SNS activity
RAAS
myocardial hypertrophy

119
Q

what are some causes of heart failure

A

impaired cardiac function (MI, valvular disease)

excessive work demands (HTN, anemia, excessive IV fluids)

120
Q

define congestive heart failure

A

failure of the heart as a pump with accompanying congestion of body tissues

generally creates a positive feedback mechanism that progressive worsens

121
Q

what is the most common mechanical complication of MI

A

left sided heart failure

122
Q

outcomes of heart failure

A

decreased cardiac output and pulmonary congestion

leads to…
activity intolerance/signs of decreased tissue perfusion
impaired gas exchange
pulmonary edema

123
Q

how does anemia cause high output failure

A

impaired O2 delivery -> tissue hypoxia -> catecholamines, increased HR and SV, increased cardiac output

124
Q

how does beriberi cause high output failure

A

impaired cardiac metabolism and decreased SVR -> impaired O2 delivery -> tissue hypoxia -> catecholamines, increased HR and SV, increased cardiac output

125
Q

how does sepsis cause high output failure

A

decreased svr and fever -> excessive tissue O2 demands and impaired O2 delivery -> tissue hypoxia -> catecholamines, increased HR and SV, increased cardiac output

126
Q

how does hyperthyroidism cause high output failure

A

increased basal metabolic rate -> excessive tissue O2 demands -> tissue hypoxia -> catecholamines, increased HR and SV, increased CO

127
Q

define shock

A

systemic hypoperfusion caused by either a reduction in CO or in the effective circulating blood volume

CV collapse

128
Q

what are the types of shock

A

hypovolemic
obstructive
distributive

129
Q

what is hypovolemic shock

A

loss of whole blood, plasma, of extracellular fluid

130
Q

what is obstructive shock

A

inability of the heart to fill properly (cardiac tamponade)

obstruction to outflow from the heart (PE, dissected aneurysm)

131
Q

what is distributive shock

A

loss of sympathetic motor tone
presence of vasodilators (anaphylactic shock)
presence of inflammatory mediators (septic shock)

132
Q

shock flow chart

A
133
Q

what are some complications of shock

A

ARDS
acute renal failure
GI complications
DIC
MODS (multiple organ dysfunction

134
Q

what is the leading cause of death in the first year of life

A

congenital heart defects

135
Q

what causes congenital heart defects

A

prenatal environment
genetic risk factors
maternal rubella
insulin dependent diabetes
alcholism
phenylketonuria (PKU)
hypercalcemia
drugs
chromosomal aberrations

136
Q

how are congenital heart defects classified

A

on blood flow:
lesions increasing pulm blood flow
lesions decreasing pulm blood flow
obstructive lesions
mixed lesions

137
Q

describe lesions that increase pulm blood flow

A

Patent arterio ductus

defects that shunt blood from high pressure to low pressure (left to right) with pulm congestion and acyanosis

138
Q

describe lesions that decrease pulm blood flow

A

generally complex with right to left shunt and cyanosis

tetralogy of Fallot
VSD
tricuspid atresia
right ventricular hypertrophy
pulm valve stenosis

139
Q

describe obstructive lesions

A

right or left sided outflow tract obstructions that curtail or prohibit blood flow out of the heart
no shunting

coarctation aorta
aortic stenosis
pulm valve stenosis
hypoplastic left heart syndrome

140
Q

describe mixed lesions

A

desaturated blood and saturated blood mix in the chambers or great arteries of the heart

transposition of the great arteries
trunkess arteriosis

141
Q

what are common consequences of congenital heart defects

A

heart failure- neurohumoral and hemodynamic changes create abnormal ventricular wall stress and cause the myocardium to hypertrophy

hypoxemia

142
Q

define hypoxemia

A

arterial O2 tension is below normal and results in low O2 arterial saturations and cellular function alteration

143
Q

define cyanosis

A

blue discoloration of mucous membranes and nail beds

result of deoxygenated hemoglobin

144
Q

clinical manifestations of heart failure in peds

A

poor feeding/sucking=leads to failure to thrive
dyspnea
tachypnea
diaphoresis
retractions
grunting
nasal flaring
wheezing
coughing
pallor or mottling
hepatomegaly

pulm overcirculation: predominant cause associated with congenital defects

145
Q

what is Eisenmenger syndrome

A

pulmonary vascular resistance increases that exceed or equal vascular resistance

results in a reversal of shunting

146
Q

what defects cause hypoxemia and cyanosis

A

lesions that cause obstruction and shunting from right to left (ex: tetralogy of fallot)

defects involving the mixing of saturated and unsaturated blood (ex: univentricular heart)

transposition of the great arteries

147
Q

clinical manifestations of mild hypoxemia

A

cyanosis only occasionally when stressed

148
Q

clinical manifestations of severe hypoxemia

A

feeding intolerance
poor weight gain
tachypnea
dyspnea

149
Q

clinical manifestations of chronic hypoxemia

A

small for their age
cognitive/motor skill delays
polycythemia
sob with exertion
easily fatigued
exercise intolerance
clubbing of the nail beds

150
Q

lesions increasing pulm blood flow

A

left to right shunt
presents like a cyanotic CHF

ex:
PAD
atrial septal defects
ventricular septal defect
complete atrioventricular canal defect
tetralogy of fallot
tricupsid atresia

151
Q

lesions that decrease pulm blood flow

A

right to left shunt
presents cyanotic

ex:
tetralogy of fallot
tricuspid atresia

152
Q

obstructive lesions

A

no shunt
present as low CO and shock

ex:
coarctation of the aorta,
hypoplastic left heart
aortic stenosis
pulmonary stenosis

153
Q

mixed lesions

A

variable shunts
variable presentation

ex:
transposition of great arteries
total anomalous pulm venous conection
truncus arteriosus

Pathophysiology (3 decks)

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