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cvs Flashcards

1
Q

what is the portal vein composed off

A

The Superior Mesenteric Vein joins the

Splenic vein to form the Portal vein

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2
Q

wha consists of femoral triangle

A

y near femoral
triangle (inguinal lig [sup], sartorius [lat],
adductor longus [med]

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3
Q

popliteeal fossa pathologies

A

popliteal artery vein with tibial nerve, aneurysms and baker cyst

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4
Q

aortic isthmus inury

A

Aortic isthmus (tethered by ligamentum
arteriosum) is more commonly ruptured
ascending aorta rare

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5
Q

where is the coronary sinus located?

A

course through the coronary
sinus, which resides in the AV
groove on the posterior aspect of
the heart

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6
Q

location of av node

A

AV node
• Right atrium near septal cusp of tricupsid
valve near coronary sinus

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7
Q

how to treat a flutter

A

Isthmus between the IVC and
tricuspid annulus is site of ablation for A
Flutter

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8
Q

2 manifestation of subclavian steal sbdrome

A 
ischemia in the affected extremity
(eg, exercise-induced fatigue,
pain, paresthesias) or
vertebrobasilar insufficiency (eg,
dizziness, vertigo).
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9
Q

what does the azygous vein drain

A

Posterior mediatinum immediately to the

right of the midline

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10
Q

heart borders

A

Anterior surface: RV
• Inferior surface: RV + LV touching
central tendon
• Posterior surface: LA

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11
Q

stab wound to vertebral body, ad pulmonary trunk

A

stab to rght veretebral body=IVC affected

2nd intercosal left sternal border, pulmonary trunk

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12
Q

what embro structure gives rise to sinus venosus

A

cardinal veins

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13
Q

what if there is cannulation above the inguinal ligament?

where does femoral artery lie?

A 
Cannulation above the
inguinal ligament can
significantly ↑ the risk of
retroperitoneal hemorrhage.
femoral arterylies below the peritoneum
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14
Q

Paracolic gutters

A

Right paracolic gutter (between ascending
colon and abdominal wall): fluid
accumulation > think GI organ issue

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15
Q

pcwp cathether

A

ballon occludes bf through artery mesures lv/la pressure=endiastolic volue

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16
Q

hw to access the left side of heart

A

CVCs must cross the
interatrial septum at the site of the
foramen ovale

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17
Q

patents with ricuspid regugation leads to what complication

A

often leading to septic

pulm emboli.

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18
Q

what is the crista terminalis

A

Crista terminalis: separates smooth sinus

venosus and pectinate muscles

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19
Q

If i have a thrombus at the left venticle why do i have decreased CO?

A

LV mural thrombus: systolic dysfunction >

impaired apical wall movement

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20
Q

what forms diphragmatic surface of heart

A

The inferior wall of the LV forms
most of the inferior
(diaphragmatic) surface of the
heart and is supplied by the PDA=av node

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21
Q

papillary muscle rupture

A

The posteromedial
papillary muscle is supplied
solely by the PDA, making it
susceptible to ischemic rupture

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22
Q

why posteromedial more common to rupture

A

it has single blood supply whereas the anterior one dual blood supply therefore PM more common

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23
Q

what is the conus artery

A

early branch of RCA supplies Aner IV septum and conus of pulmonary artery

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24
Q

a person with infantile thiamine deficiency presents with

A

2-3 months after birth

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25
Q

what is persistent foramen ovale

A

Failure or septum primum and septum

secundum to fuse

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26
Q

what murmur does bicuspid stenosis have and what are the risks of bicuspid stenosis

A

• Early systolic, high frequency click
• Increased risk of stenosis, insufficienc
and infection
susceptible to infection

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27
Q

presntation of RF

A

MR early, MS late

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28
Q

compare acute heart rejection with chronic

A 
Chronic rejection
• Scant inflammatory cells with interstitial
fibrosis
Acute transplant rejection
• Weeks after surgery
• Dense infiltrate of mononuclear cells
(mainly T cells)
• T cell sensitization against graft MHC Ag
Hyperacute
sudden cessation of blood flow
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29
Q

what are the cardiac complication of staph endocarditis

A

Perforate heart valves, rupture chordae
tendineae, send septic emboli to lung or
brain

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30
Q

what causes entrococcus

A

GU
instrumentation or catheterization
has been a/w enterococcal
endocarditis.

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31
Q

surgical procedures with strep nesieria

A

Bactermia after nasal polyp removal

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32
Q

what does strep viridans cause

A

deep wound infections, abdominal
abscesses and septicemia
Dextrans adhere to tooth enamel and
fibrin platelet aggregates

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33
Q

anterior uveitis caused by

A

HSV, Syphilis, Lyme disease

• HLa B27

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34
Q

erythema nodsum caused by

A

GAS, S Aureus, cocci, histo, blasto,

chlamydia, crohns, sarcoid

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35
Q

what is the function of subendothelial colalge in subacute BE

A

subendothelial collagen is important for

platelet adhesion, not bacterial

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36
Q

how to prevent cathether induced infection

A 
S Aureus and S epi are common
infections
Reduction in CVC infection
• Hand watching
• Chlorhexidine skin disinfection
• Sterile procedure
• Subclavian or internal jegular insertion >
femoral
• Remove ASAP
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37
Q

how do patients with coarctation of aorta die

A

HTNassoc
complications, incl LV
failure, ruptured dissecting AA,
and SICH.

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38
Q

what causes sudden intracranial spontaneus hemorhhage

A

AVM, ruptured cerebral aneurysms,
abuse of cocaine
• Can also be due to coaractation of the
aorta

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39
Q

what does an unstable arthersclerotic plaqye consist off

what causes risk of rupture

A 
eg, that w/ active inflammation,
a lipid-rich core, a/o a thin fibrous
cap)
Fibrous cap over athero plaque thins >
risk of rupture Larger lipid rich core of
athero > risk of rupture
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40
Q

how is calcification associated with rupture, and macrophages as well?

A

Macrophages secrete metalloproteinase
which thin fibrous cap of athero
Statins decrease inflammation of athero >
stabilzes plaque
• More calcification of coronary artery >
the greater the risk of rupture

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41
Q

Hibernating myocardium

A 
Hibernating myocardium refers to
the presence of LV systolic
dysfxn due to ↓ coronary blood
flow at rest that's partially or
completely reversible by coronary
revascularization.
lowers
myocardial metabolism and function to
match blood flow preventing necrosis.
Disorganized contractile and
cytoskeletal proteins, altered adrenergic
contril and increased Ca2+ response >
decreased contraction. Coronary
revascularization and return of flow will
improve contractility and LV functio
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42
Q

what is ischemic preconditioning

A

Ischemic preconditioning: repeated brief
ischemic events protect myocardium from
subseqent prolonged ischemia

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43
Q

systemic embolization of endocarditis

A

erebral, pulmonary or

splenic

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44
Q

how does diffuse proliferative gn look

A

which
is Chx by diffuse thickening of
the glomerular capillary walls w/
“wire-loop” structures on LM.

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45
Q

explain dermatomyositis

A

Extramuscular: interstitial lung disease,

vasculitis and myocarditis

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46
Q

how does renal invovement of bacterial endocarditis present

A

septic emboli, or glomeularnephritis due to development of immune complex

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47
Q

what are cardiac manifestations of lupus

A 
smallvessel
necrotizing vasculitis,
pericarditis, and Libman-Sacks
endocarditis (small, sterile
vegetations on both sides of the
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48
Q

carcinoid valvular manifestations

what can carcinoid tumor ca secrete

A

TIPS(tricuspid insufficiency;/pulmonary stenosis)Can secrete histamine, serotonin and VIP

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49
Q

Hypertrophic cardiomyopathy-LVOT leads to rg

type of murmur

A

exacceberate obstruction and cause rg
Harsh systolic crescendo decrescendo
murmur > worsens
with valsalva, standing up or nitro

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50
Q

what is Endocardial thickening and
noncompliant ventricular walls
what is Patchy fibrosis in the mural endocardium:

A

restrictive cmo

chronic ischemic heart disease

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51
Q

Arrhythmogenic Right Ventricular

Cardiomyopathy

A

Mutation of Ca binding sarcoplasmic
reticulum protein
• Progressive fibrofatty change in
myocardium

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52
Q

pain of pericarditis positional pain

A 
may be exacerbated
by swallowing or coughing
inflammatory rxn to cardiac
muscle necrosis that occurs in the
adjacent pericardium.
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53
Q

location of acute pericarditis

A

Sharp, pleuritic pain that is exacerbated
by swallowing (suggests posterior
pericardium involvement) and radiating to
neck (suggest inferior pericardium
involvement)

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54
Q

condition for acute pericarditis to occur

A

Must have transmural necrosis

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55
Q

presnetation of dresseler syndrome

A

Fever, pleuritis, leukocytosis, pericardial
friction rub, new pericardial or pleural
effusion

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56
Q

viral myocarditis

A

lymphocytic interstitial inflammatory

infilitrate

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57
Q

Hypersensitivity myocarditis

A

Interstitial inflammatory infiltrate or
mononuclear inflammatory cells and
eosinophils

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58
Q

signs of constrictive pericarditis

A

↑ JVP, pericardial knock,
pulsus paradoxus, and a
paradoxical ↑ in JVP w/
inspiration (Viral, surgery, radiation or TB

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59
Q

what is a sign of irreversbile myocardial infarction

A

mitochondrial vacoulization
irreversbile injury-Mitochondrial vacuoles and phospholipid
containing amorphous densities
revers

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60
Q

how does reversible injury look like

A 
Myofibril relaxation
• Disaggregation of polysomes
• Disaggregatiuon of granular and fibrillar
elements of the nucleus
• Nuclear chromatin clumping
• Triglyceride droplet accumulation
(especially in hepatocytes)
• Glycogen loss ( rapid loss of cunction0
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61
Q

In acute mi what sort is changed

A

thinning, and fibrous healing of the infarcted zone of myocardium. Regional dysfunction of the infarcted myocardium causes volume overload for the remaining viable myocardium. The net result is usually eccentric hypertrophy, with enlargement of the LV cavity.

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62
Q

what is peripheral pulmonary artery stenosis

A

Pulmonary stenosis: innocent murmur due
to hypoplasia of branch pulmonary arteries
• Low grade, mid systolic, high pitch
blow murmur

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63
Q

systemic sclerosis associated diseases

A

Cor pulmonale, pericardial dz,
myocardial fibrosis and conduction system
disease

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64
Q

when do we see mitral valve calcificaition

A

Mitral valve calcification is usually around
the annulus, seen in women over 60, and
asymptomatic

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65
Q

wha cardiac pathology rheumatoid arthiritis can cause

A

Can cause pericarditis or myocarditis

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66
Q

what is ortner syndrome

A

MS > LA dilation > compresses L
recurrent laryngeal nerve (neurapraxia)
leading to hoarseness

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67
Q

where does recurrent laryngeal nerve innv

A

Innervates all laryngeal muscles except

cricothyroid

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68
Q

what are other causes of hoarsness

A 
Laryngeal edema
• Vascular disease
• Laryngeal mucosal disease (epi
sloughing)
• Vocal cord polyps
69
Q

which drugs cause myocarditis

viral myocarditis

A

loops, thiazides, ampicillin, azithromycin

PAC

70
Q

What causes syncope on aortic stenosis
and cyanosis on TOF
AR

A

excercise, causes vasodilation therefore decrease in blood flow no compensation in increased co
caused by infective endocarditis

71
Q

mcc of cardiogenic shock in ami

A

From massive LAD MI

72
Q

what are pericytes

A

Pericytes are pluripotent cells in

postcapillary venules

73
Q

explain details of artherosclerosis

A 
Endothelial damage increases expression
of surface vascular celL adhesion
molecules allowing adhesion and migration
of monocytes into the intima. Macrophages
release PDGF, FGF, endothelin 1 and IL 1
causing migration/proliferation of
vascular smooth muscle cells within the
INTIMA. Smooth muscle cells synthesize
collagen, elastin and proteoglycans
forming the fibrous cap.
• Macrophages release MMP that
degrade the fibrous cap
increasing vulnerability to rupture
74
Q

Where does Arthero first occur in teens

what increases the likelihood of AS rupture

A

abdominal aorta
plaque stability rather
than plaque size or the degree of
luminal narrowing.(macrophages secrete metalloproteinases) decrease plaque sabuklity

75
Q

function of Procollagen peptidase

A

cleaves terminal ends in ehler darlos

76
Q

what causes onion skinning

A

rteriolar walls due to layers of smooth muscle cells and reduplicated basement membrane is seen in hyperplastic arteriolosclerosis, which can occur in severe chronic hypertension

77
Q

what is malignant nephrosclerosis

A 
fibrinoid
necrosis and hyperplastic
arteriolosclerosis ("onion-skin"
appearance). A MAHA can occur
due to erythrocyte fragmentation
and platelet consumption at the
narrowed arteriolar lumen.
78
Q

symotoms of accelerated hypertension

A

Retinal hemorrhage, exudates or

papilledema

79
Q

thromboangities obliterans

give histology of every vasuiliti

A

Vascultiis of Radial and Tibial arteries
• Thrombosing vasculitis that extends into
contiguous veins and nerves

80
Q

what is leukocytoclastic vascutis

A 
Leukocytoclastic vasculitis
• Microscopic polyangitis, microscoping
polyarteritis, hypersensitivity vasculitis
(RA)
• Segmental fibrinoin necrosis of small
vessels
• Similar to PAN
81
Q

if a patient presents with TA can manifest as audible bruits, blood pressure discrepancies, pulse deficits, and distal ulcerations

A

it is generally large vessel involvement

82
Q

histology of renal artery stenosis

A

crowded glouemerli due to atrophy since kidney shrinks

83
Q

Aortic aneurysm in marfans syndrome

A

Fragmentation of elastic tissue and
separation of elastic and fibromuscular
components of tunic media, cleft like space
filled with amorphous extracellar matrix

84
Q

aquired cause of marfans syndrome due to

A

Beta aminopropionitrile

85
Q

epidemology of AAA

characterised by

A 
Over 60
• Smoking
• HTN
• Male
transmural inflammation
infrarenal abdominal aorta lacks vasa
86
Q

pathogenesis of aortic dissection descendiong aorta

A

HTN is largest risk factor > vasa
vasorum occlusiong > decreased blood to
media > degenerates SM in media +
increased wall stiffness > tear

87
Q

what is chronic venous insuff complication

A

Painful thromboses, stasis dermatitis, skin
ulcerations (common over medial
malleolus), poor wound healing and
superficial infections

88
Q

Phlegmasia alba dolens

A

Phlegmasia alba dolens: result of
iliofemoral venous thrombosis in
peripartum women

89
Q

celiac disease coagulopathy

A

Risk of hemorrhagic diathesis(vit k Deficiency)

90
Q

hypothyrodism coagulopathy

A

associated with cerebral venous thrombosis

91
Q

lymphedema

A

Obstruction of lympoid capillaries
• Marked swelling of dorsum of distal limb
• Initially soft and pitting but eventually
becomes firm and nonpitting > leads to
fibrosis of skin

92
Q

what is the exact pathology of mvp

A

Proliferation of spongiosa in leaflets,
fragmentation of elastin fibers with
increase mucopolysaccharides and type 3
collagen deposition

93
Q

how does rash spread in kawasaki

A

Rash on extremities that spreads

centripetally to trunk

94
Q

endocardial fibrosis =restrictive

A

characterized by thickening and fibrosis of

apical endocardial surface

95
Q

how to diagnose atrial myxoma

A 
obstruction +constitutional symotoms
mucopolysaccharide
stroma and abn blood vessels w/
hemorrhaging.
Can met to the heart
• Will see pancytopenia, weakness, fatigue,
ecchymoses
96
Q

how does ADHF presents

A

Sudden onset of SOB with orthopnea,
pulmonary edema, dilated heart > this
Acute Decompensated HF

97
Q

how is coostochondritis classified dy/dx from pleural and pericardial

A 
reproducible w/ palpation and
worsened w/ movement or
changes in position.
Pleural or pericardial pain
• Worsens with inspiration
98
Q

what is the bp difference in aortic dissection

A

Aortic dissection

• Usually a difference of > 10 in each arm Subendocardial granulomatous lesions with fibrinoid necrosis

99
Q

RF histopath

A

Subendocardial granulomatous lesions with fibrinoid necrosis

100
Q

WE have an MI with acute Mitral regurg, how do you differentiate between papillary muscle dysfunction and chordae tendinae

A

papillary muscle dysfunction is associated with ischemia which later resovles however chordae tendiae not associated with ischemia
myxomatous mitral valve disease (mitral valve prolapse), rheumatic fever, or endocarditis.

101
Q

when thinking about mitral regurg think anatomically

A

anulus
paipillary muscle dysfunction and displacement
chordae tneinae
and the valve itself

102
Q

chronic lymphedema

A

due to poor lymphatic drianage in malignancy

never use diuretics

103
Q

peripartumo CMO

A 
Peripartum cardiomyopathy is a
relatively uncommon cause of
DCM that may be related to
impaired fxn of angiogenic GFs.
DCM involves compensatory
eccentric hypertrophy, which ↑
ventricular compliance and also
allows for temporary maintenance
of CO. Over time, ovewhelming
wall stress leads to LV failure w/
↓ EF and SSx HF
104
Q

cardiac manifestation of lyme disease

A

complete AV conduction block
are likely to have dyspnea,
lightheadedness, or syncope.

105
Q

how does thoracic aortic aneurysm present as

A

compression of different structures

106
Q

explain aortic dissection and what is the predeposition of it

A

Aortic root disease

predisposes to AD

107
Q

myocardial stunning

A

When ischemia lasts less than 30
min, restoration of blood flow
leads to reversible contractile
dysfxn

108
Q

pathophys of heart acting on ischemia

A

Heart will stop beating in 60 seconds
• Although there is still ATP around, ATP
in locations of high metabolic demand is
rapidly depleted and causes heart to stop
Ischemia less than 30 min > reversible
damage

109
Q

a young patient comes with DCM what do u suspect

A

viral myocarditis
Direct viral injury and autoimmune
rxn > inflammation > dialtion and systolic
dysfunction

110
Q

how can i atteunate or silence a murmur in HCOM

talk about pathophsy of restrictive heart disease

A 
Decreased preload or decreased
afterload increase obstruction and murmur
> standing up would make murmur louder
• Increaed preload or afterload will
make murmur quieter >
squatting
Diastolic HF is caused by ↓
ventricular compliance and is
characterised by normal LV EF,
normal LV EDV, and ↑ LV filling
pressures. HTN, obesity, and
infiltrative disorders
111
Q

compare pressures of systolic hf and diastolic hf

A 
Diastolic HF
• Normal EF
• Normal end diastolic volume
• Increased LV filling pressure
• Decreaed LV compliance
Systolic HF
• Decreased EF
• Increaed end diastolic volume
112
Q

a person has a vsd what will be the oxygenation of the right heart

A

Right atrial SpO2 remains normal with VSDs of any size, unless tricuspid regurgitation is also present

113
Q

pulse patterns een in HCOM

A

Bifid carotid pulse with brisk upstroke

indicated HOCM

114
Q

most likely pathways of paradoxical embolism

when does paradoxical embolism occur

A 
DVT through PFO, VSD, ASD or
pulmonary arteriovenous malformation to
brain
can facilitate
paradoxical embolism due to
periods of transient shunt reversal
(eg, during straining or
coughing).
115
Q

what is associated with marfans
what is marfans habitus
talk about eissengmer syndrome

A

Early-onset CMD of the

aorta predisposes to AD

116
Q

when does murumur intesity of AORTIC REGURGTATION OCCUR, and mitral stenosis how does it vary with opening snap

A 
The worse the stenosis, the higher the
residual pressure in the L atrium causes a
louder and earlier opening snap
presystolic accentuation
of the MS murmur disappears
117
Q

explain how mitral stensosis causes tricuspid regurgtation

A

Right ventricular dilatation can occur in MS when the resulting pulmonary hypertension is severe enough to cause right heart failure. Tricuspid regurgitation can occur as a complication of right ventricular dilatation.

118
Q

compare acute AR with chronic AR

A

impaired LV contracility late onset of AR
Small SV
LV Dilation
• Small SV and low PP

119
Q

Talk about the murur of aortic stenosis,

and aortic pressure gradient

A 
st heart sound and
typically ends before the A2
component of the 2nd heart
sound.
Large difference in pressure between LV
and aortic pressure
• Crescendo decrescendo murmur (loudest
mid systole > large difference in pressure)
120
Q

when is S3 normal and abnormal

A

Normal in children, young adults and
pregnancy
over 40, HF, restrictive
cardiomyopathy, high output states

121
Q

when is s4 abnormal

A

Abnormal: younger adults, children,
ventricular hypertrophy, acute MI
Normal in healthy older adults

122
Q

places with increased metastatic calcification

A

(especially in alkaline environement of
kidneys, lungs, arteries
and gastric mucosa

123
Q

serotonin

A

Produced by platelets

• Vasodilation and increased premeability

124
Q

where is prostaglandin I@ secreted from

A 
Prostacyclin (prostaglandin I2) is
synthesized from prostaglandin
H2 by prostacyclin synthase in
vascular endothelial cells. Once
secreted, it inhibits platelet
aggregation and causes
vasodilation to oppose the fxns of
thromboxane A2 and help
maintain vascular homeostasis.

Damaged endothelium decreased
PGI2 synthesis and TXA2 predominates >
occlusion

125
Q

mitral valve regurg explain forward vs backward flow

A 
Forward SV: blood in aorta
• Backward SV: blood into LA
• Amount of backward SV is related to
afterload (decreased afterload will decrease
backward SV)
Decreased HR > higher EDLVV > worse
backward SV
• Same as increase preload (if MR is
volume dependent)
• Increase contractility will wrosen
backward SV
126
Q

explain the hormonal variations of raas in the raas system

A 
Increase Renin from JG cells
• Angiotensin (made by liver) > ang 1
(renin) in sysemic circulation
• Ang 1 > ang 2 (angiotensin converting
enzyme) in the lung
• This means higher ang 2 than ang 1 in the
pulmonary vein
127
Q

why edema is late in HF

A 
In chronic heart failure,
increased lymphatic drainage
initially offsets factors favoring
edema, whereas acute changes
(eg, venous thrombosis, heart
failure decompensation) are more
likely to produce edema
128
Q

explain pulsus paradoxus and its causes

A

MCC of pulses paradoxus in absence

of pericardial disease

129
Q

aortic stenosis variation in age, then marfans syndrome causing AR, where is MVP heard

A 
Under 60 > think bicuspid aortic valve or
rheumatic heart disease
• Over 60 > calcification due to wear and
tear
Marfans
• Aortic dilation > AR
• Aortic dissection
MVP
• Mid systolic click @ cardiac apex
130
Q

what is the most common cause of AR in a young patient

A

he most common cause of chronic AR in a young patient is a congenital bicuspid valve. Bicuspid valve is also a common cause of early-onset aortic stenosis.

131
Q

a person comes with angina given nitroglycerin why pain improves

A

simple venous pooling of blood

132
Q

what is athletes heart

A 
There's predominant
eccentric hypertrophy w/ a
smaller component of concentric
hypertrophy, leading to an overall
↑ in LV mass, enlarged LV cavity
size, ↑ LV wall thickness, and ↓
resting HR.
133
Q

sick sinus syndrome

A 
ECG
typically demonstrates
bradycardia w/ sinus pauses
(delayed P waves), sinus arrest
(dropped P waves), and jxnal
escape beats.
Cardiovascular (CV) Pathophysiology
(Patp)
2
15650 Acute heart failure Pts w/ DHF have ↑ LV EDP and
134
Q

one cause of TR regurg

A 
Severe TR can lead to right-sided
HF, evidenced by JVD,
hepatomegaly, lower extremity
edema, and the absence of pulm
edema. Permanent PM placement
can cause TR b/c the RV lead
passes through the TV orifice and
can disrupt valve closure
135
Q

triggeres of prizmental angina

A 
Possible triggers are cigarette
smoking, cocaine/amphetamines,
and dihydroergotamine/triptans
Stimulates both alpha receptors and
serotonin receptor
136
Q

what responses to precapillary sphincters

A 
Precapillary sphincters
• Respond to NE and epi
• Dilate with histamine, hypoxia, high
CO2, and acidosis
Arterioles: dilate with alpha1 blockers and
CCB
137
Q

why isorbide dinatrate has low bioavalibility

A

Isosorbide dinitrate has a low
bioavailability due to extensive
1st-pass hepatic metabolism prior
to release in systemic circulation

138
Q

contraindications of nitrates

A

Avoid in hypertophic cardiomyopathy,

RV infarct, and with Sildenafil

139
Q

dynamic hocm obstruction which drugs avoided

A

which can be caused
by ↓ in cardiac preload a/o
afterload. Therefore, Rx that ↓
venous return or SVR

140
Q

which drug is useful in hypertension with resting bradyardia

A

nifedipine is the most appropriate agent to manage hypertension as it has minimal effect on cardiac conduction. Dihydropyridines can cause reflex tachycardia in response to peripheral vasodilation and are therefore useful in hypertensive patients with resting bradycardia.
also pindolol

141
Q

benefit of milirone

A

PDE3 inhibitor > increased cAMP >
vasodilation and increased cardiac
contractility

142
Q

antiarrythmic drugs which have less use dependance

A

1C > 1A > 1B
• The more they are used, the longer the
drug binds

143
Q

adverse effects of substance p

A

Mediated pain > topical capsaicin can

cause depletion of Substance P

144
Q

contraindications of ocps

A 
OCPs are: prior Hx of TE event
or stroke, Hx of an oestrogendependent
tumour, women over
age 35yrs who smoke heavily,
hypertriglyceridaemia,
decompensated or active liver
disease (would impair steroid
meta), preg.
145
Q

how do ocps work

A 
Estrogen: suppresses GnRH
• Progesterone: decreases risk of
endometrial cancer and thickens cervical
mucus
• Adverse: breakthrough menstrual
bleeding, breast tenderness, weight gain,
DVT, PE, stroke and MI
146
Q

amidarone effects

A

Corneal micro deposits
• Optic neuropathy
• Peripheral neuropathy

147
Q

how does spirnolactone work

A

Block deleterious effect of aldosterone on
heart > regression of fibrosis and improved
ventricular remodeling
• Improves survival in CHF with low
EF

148
Q

why nsaids cause hyperkalemia

A

So NSAIDs would inhibit prostaglandins —> decrease renin levels —> decrease aldosterone —–> decrease sodium reabsorption and potassium excretion —–> hyperkalemia

149
Q

what drugs cause hyperkalemia

A 
Non selective Beta blockers: no K into
cells
• ACE inhibitors: no aldosterone
• ARBs: no aldosterone
• K sparing diuretics
• Digoxin: inhibit Na/K pump
• NSAIDs: reduced renin and aldosterone
secretion
150
Q

drugs causing sexual dysfunction

A

SSRI, TCA, thiazide, spironolactone,

clonidine

151
Q

mechanism of omega 3

A

decreased ffa to liver increase synthesis of enzyme

152
Q

which drug lowers tags

A

omega/fibrates bile acid sequesterantsLowers LDL but increases TAG

153
Q

Physical exam finding on cor pulmonale

A

Accentuation and splitting of S2, JVD,

hepatomegaly

154
Q

how to prevent skin necrosis

A

Tissue
necrosis is best prevented by local
injection of an α1 blocking drug,
such as phentolamine.

155
Q

causes of orthostatic hypotension

A
  • Diuretics
  • Diabetes
  • Parkinsons
  • Hyperglycemia
156
Q

other effects of alpha 2

A

Decreased lipolysis
• Decreased NE release
• Increased platelet aggregation

157
Q

which drugs cause DILE

A

HEAPS ENTERACEPT

158
Q

explain inhibitios of raas
Hyperuriceia in TZDS
mechanism of action of spirnolactone, and amiloride

A

which results in ↓
vasoconstriction and ↓ renal Na
and water retention

Hyperuricemia: increase reabsoprtion in
PCT

Add spironolactone to spare K in late
DCT and early collecting duct
• Causes downregulation of ENaC and
Na/K pumps
• Amiloride and triamterene block ENaC
on principal cells
159
Q

how does omega 3 work

A

Omega 3 FA: decrease VLDL

production,

160
Q

what is the pathophys of thomboisis obliterans

A

we have vasuclitis and then results in thrombosis typically occurs in young smoker

161
Q

clinical presentation of popliteal artery aneurysm

A

An aneurysm of the popliteal artery. Can present with obstruction and ischemic symptoms of the lower leg and foot.

162
Q

what drug reduces the frequency of angina episodes

A

it is always a beta blocker

163
Q

what drug reduces the frequency of angina episodes

A

it is always a beta blocker
Though β-blockers also inhibit adrenergic-mediated coronary vasodilation, the resulting increase in coronary vascular resistance is overcome by the reduction in heart rate, which improves coronary perfusion by prolonging diastole.

164
Q

infective endocarditis when would u do a ct angiogram

A

if he has symptooms of pulmonary embolism

165
Q

how do you diagnose HOCM

A

typically shows systolic anterior motion of the anterior mitral valve leaflet, asymmetrical septal hypertrophy, and septal wall thickness of >15 mm.

166
Q

A person comes with HYpokalemia,HTN, what are the different possibilities

A

aldoesttonism, RAS, fibromuscular dysplasia

167
Q

How to diagnose heparin induced thrombocytopeni

A

. This adverse event most commonly manifests with venous or arterial clotting 5–14 days following heparin administration;

168
Q

explain pathophys of ASD

A

ostium secundum =excess apoptosis

septum primum doesnt migrate work=failure of neurocrest apoptosis behind secundum

169
Q

why in vsd no split

A

With ASD, you get the blood flow as you described leading to fixed splitting.

With VSD, you get wide splitting (not fixed) and there is delayed P2 . However it is not “fixed” because, over time the VSD allows the pressures in the LV and RV to equalize, such that there is not as much blood flowing into the RV as compared to the amount from the ASD. Im assuming the pressures dont normalize in the atrium as they would in the ventricles.

usmle (38 decks)

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