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Cardio Flashcards

1
Q

^ contractility (&SV)

A 
Big picture
    1. ^intracellular Ca
    2. ^ sarcomere length
-Catecholamines
    Inhibit phospholamban --> ^Ca into SR 
-^intracellular Ca
-Decrease extracellular Na
    (decrease Na/Ca exchanger)
-Digitalis
    blocks Na/K pump --> ^ intracellular Na --> stops Na/Ca exchanger (too much Na to bring in more) --> ^ intracellular Ca
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2
Q

Decrease Contractility (& SV)

A
  • B1 blocker (decrease cAMP)
  • Systolic HF
  • Acidosis
  • Hypoxia/hypercapnia
  • Non-dihydropyridine CCB (verapamil, diltiazem)
  • loss of myocardium (MI)
  • dilated cardiomyopathy
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3
Q

Decrease pre-load

A

PrE-load = VEnodilators
-nitroglycerin
ACEi, ARB: pre & after

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4
Q

Decrease afterload

A

Afterload= VAsodilators (hydralazine)

ACEi, ARB: preload & afterload

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5
Q

Pompe Disease

A 
=Type II glycogen storage dz
-primarily affects heart: "Pompe trashes the pump"
-Lysosomale a-1,4-glucosidase deficiency 
    -fxn: hydrolysis of glycogen branches
    -->glycogen deposits in myocardium
6mo:
  -developmental delays
  -feeding probs
  -HF
  -hypotonia
  -hepatomegaly
  -Biventricular hypertrophy
      -short PR interval, wide WRS
  -^Serum creatine kinase
  -decreased leuk acid maltase
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6
Q

Fabry Disease

A

Lysosomal storage dz

  • a-galactosidase deficiency
    • ->ceramide trihexoside accumulates
  • Peripheral neuropathies: hands & feet
  • *Angiokeratomas (benign cutaneous lesion of caps)
  • CV dz
  • renal dz
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7
Q

Gaucher Disease

A 
Lysosomal storage dz
B-glucocerebrosidase deficiency
-hepatosplenomegaly
-aseptic necrosis of femur
-bone crises
-Gaucher cells
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8
Q

Large Vessel Vasculitis

A 
Giant cell (temporal) arteritis
Takayasu Arteritis
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9
Q

Giant cell (temporal) arteritis

A 
-Mostly affects br of carotid artery
Epidemiology/Presentation:
    -elderly females
    -unilateral headache (temporal a)
    -jaw claudication
    -possible permenant blindess (ophthalmic a)
Labs/path:
   -focal granulomatous inflam
   -^ESR
Tx:
   -Corticosteroids 
    Tx before biopsy to prevent blindness
Asc: polymyalgia rheumatica (inflam disorder, muscle pain & stiffness)
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10
Q

Takayasu Arteritis

A

Granulomatous thickening & narrowing of aortic arch & great vessels
Presentation/Epidemiology:
-Asian females,

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11
Q

Medium Vessel Vasculitis

A 
Polyarteritis Nodosa
Kawasaki Dz (mucocutaneous lymph node syndrome)
Buerger Dz (thromboangiitis obliterans)
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12
Q

Polyarteritis Nodosa

A 
Presentation:
  -Youngins
  -Hep B (30%), HepC, Hair cell leuk 
  -Fever, wt loss, malaise, headache
  -GI: abdominal pain, melena
  -HTN, neuro dysfxn
  -cutaneous eruptions
  -renal damage
Path/Labs:
  -renal & visceral vesels- NOT pulm arteries
  -Immune complex mediated
  -Transmural inflammation + fibrinoid necrosis
  -Diff stages of inflam coexist in diff BV
  -Rosary sign: lots of little aneurysms
Tx:
  -corticosteroids
  -cyclophosphamide 
        (forms cross links in DNA--> apoptosis)
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13
Q

Kawaski Dz = mucocutaneous lymph node syndrome

A 
Presentation:
   -Asian children  desquamating)
   -CRASH & BURN
      -Conjunctival injection
      -Rash
      -Adenopathy (cervical)
      -Strawberry tongue
      -Hand & foot: edema, erythema
      -Fever
Complications:
   -Anneurysms
Tx:
   -IVIg
   -Aspirin (only time give kids aspirin)
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14
Q

Buerger Dz = thromboangiitis obliterans

A

=progressive; recurring inflammation; thrombosis of medium BV in LE
Presentation:
-Heavy smokers (after a big burger, you want to smoke)
-males, gangrene, autoamputation
of digits, superficial nodular phlebitis
Tx:
Smoking cessation

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15
Q

Small Vessel Vasculitis

A

Granulomatosis w/ Polyangiitis (GPA)
Microscopic Polyangiitis
Churg-strauss (eosinophilic GPA)
Henoch-Schonlein Purpura

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16
Q

Granulomatosis w/ Polyangiitis (GPA)

A 
Presentation:
  -Upper respiratory tract: sinusitis, otitis, mastoiditis
  -Lower respiratory: hemoptysis, cough, dyspena
  -Renal: hematuria, RBC casts 
Triad:
   -focial necrotizing vasculitis
   -necrotizing granulomas in lung
  -Necrotizing glomerulnephritis
c-ANCA (PR3)
Tx:
   -cyclophosphamide
   -corticosteriods
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17
Q

Microscopic Polyangiitis

A 
Necrotizing
Presentation:
   Lung, kidneys, skin- NO nasopharnyngeal (unlike GPA)
   Kidneys: pauciimune nephritis
   Skin: palpable purpura
Path/Labs:
   No granulomas
   p-ANCA (anti-myeloperoxidase)
Tx:
    Cyclophosphomide 
    Corticosteroids
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18
Q

Churg-Strauss

A 
Eosinophilic GPA
Presentation
   Lungs, spleen, heart, GI, CNS
   Lungs:
      Asthma, sinusitis 
   Skin:
      Purpura, skin nodules
   CNS:
      Neuropathy: wrist/foot drop
   Kidney:
      Pauci immune nephritis
Labs:
   p-ANCA
   ^ IgE
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19
Q

Henoch-Schonlein Purpura

A 
=most common childhood systemic vasculitis
Presentation:
  Often follows URI
   ASC: IgA nephropathy (Berger Dz)
  Triad:
      -Skin: palpable purpura legs
      -Arthralgias
      -GI: abd pain
Path:
   -Due to IgA immune complex deposition
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20
Q

Baroreceptors: increased P

A

Vagal response (carotid massage)

  • stretch baroreceptor–> ^ firing
  • ^AV node refractory period
  • decreased HR
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21
Q

Cushing Reflex

A

Response to ^intracranial P (CSF)

- ->compression of cerebral arterioles --> ischemia
- ->^cerebral PCO2 -->^ symp stimulation  - ^BP (to force blood in head) - bradycardia (initially tachy until vagal response) - respiratory depression (impaired brainstem fxn)
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22
Q

A wave meaning for JVD mapping

A

Absent a wave: A-fib
Giant a wave: RA contracting against RV resistance
-tricuspid stenosis
-RV hypertrophy
-pulmonic stenosis
-pulm HTN
-RA myxoma
Cannon a waves (large a + sharp ascent & descent)
-RA contracting against closed tricuspid valve
-jxnal arrhythmias- 3rd degree heart block

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23
Q

Tricupid Valve Endocarditis

A 
-asc: IV drug use
Bacteria:
  -S. Aureus
  -Pseudomonas
  -Candida
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24
Q

S. Aureus Endocarditis

A

=Acute endocarditis

-Vegetations: large, rapidly destroy valve

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25
Q

Strep Viridans Endocarditis

A

=Subacute endocarditis

  • Indolent presentation
  • Vegetations: Small, don’t destroy valve
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26
Q

S. Epidermidis Endocarditis

A

asc: prosthetic valve

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27
Q

E. Coli Endocarditis

A

Nosocomial endocarditis (esp urinary catheters)

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28
Q

Culture Neg Endocarditis

A
  • Coxiella Burnetii

- Bartonella spp

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29
Q

Endocarditis Symps

A 
FROM JANE
Fever
Roth spots (retinal hemorrhages w/white centers)
Osler lesions (tender)
Murmur
Janeway lesions (non-tender)
Anemia
Nail bed hemorrhage
Emboli
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30
Q

Endocarditis Complications

A

Chordae Tendinaea rupture
GN
Suppurtive Pericarditis
Septic Emboli

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31
Q

Wide Splitting (A2-P2)

A

Conditions that delay RV emptying

  • Pulm stenosis
  • RBBB
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32
Q

Fixed Splitting (A2-P2)

A

ASD

^vol that delays P2 regardless of breath

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33
Q

Paradoxical Splitting (P2-A2)

A 
Delay Aortic valve closure
-Aortic stenosis
-LBBB
P2-A2
Inspiration: P2 closes later --> paradoxically removes split
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34
Q

Aortic Stenosis

A 
=Crescendo-decrescendo systolic ejection murmur
   \+/- ejection click
-Heart @: base (esp aortic area)--> carotids
-Symps: SAD
   -Syncope (decreased flow to brain)
   -Angina (decreased flow to carotids)
   -Dyspnea on exertion
Causes:
   -BAV
   -Calcification
   -Chr. rheumatic fever
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35
Q

Tricuspid Regurg

A

Holosystolic, high pitched, blowing
Heard @: tricuspid area, radiates to R sternal border
Cause:
RV dilation
Rheumatic fever & infectiveendocarditis

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36
Q

Mitral Regurg

A 
Holosystolic, high pitched, blowing
Heard at: apex --> axilla
Cause:
   -ischemic heart dz (MI)
   -MVP
   -LV dilation
   -Rheumatic fever, infective endocarditis
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37
Q

Mitral Valve Prolapse

A

Late systolic crescendo (S2 loud & long) + mid systolic click= dun NA dun NA
Heard: apex
-Can predispose to infective endocarditis
Cause:
-myxomatous degeneration
primary
or secondary to Marfans or Ehlers-Danlos
-Rheumatic fever
-Chordae rupture

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38
Q

VSD

A

Holosystolic, harsh

Heard @ Tricupsid area

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39
Q

Aortic Regurg

A 
Early diastolic decrescendo, high pitched, blowing
Hyperdynamic pulse
Head bobbing
Wide pulse P
Cause:
  Aortic Root dilation
  BAV
  Endocarditis
  Rheumatic fever
Progresses to LHF
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40
Q

Mitral Stenosis

A

S2–> Opening snap (abrupt halt in leaflet motion)
Delayed rumbling late diastolic murmur
(^ interval btwn S2 &OS: ^ severity)
Cause:
-Rheumatic fever

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41
Q

Patent Ductus Arteriosus

A 
Continuous machine like murmur
Loudest @ S2
Heard @: L intraclavicular area
Cause:
   -Congenital rubella
   -prematurity
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42
Q

Marfans (mut)

A

Chr15: fibrillin (AD)

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43
Q

MI EKG

A

ST elevation: transmural infarct
Q: transmural infarct
ST depression: subendocardial
(NSTEMI, unstable angina)

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44
Q

Lipofuscin

A

Atrophic heart + lipofuscin accumulation –> brown atrophy
Wear & tear pigment (in eldery):
-deposits in:
-hepatocytes
-spenocytes
-myocardial cells
Composition: oxidized & polymerized membrane lipids from autophagocytosed organelles
Hematoxylin & eosin stain: brown perinuclear pigment

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45
Q

Hemosiderin

A

-hemoglobin derived
-Fe containing pigment- aggregates of ferritin
-Normal:
-small amts in macros of bone marrow, liver, etc
-Excess amts:
Due to hemochromatosis
-in: hepatocytes, cardiac, pancreatic islet cells
-Microscope:
brownish granules
Prussian blue stain: turn blue
-Cardiac complications:
-restrictive cardiomyopathy
-arrhythmias

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46
Q

Dig Tox

A 
Cause:
   -Quinidine (Class IA)
Signs/Symps
   Nausea/Vomiting
   Atrial tachycardia
   AV block
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47
Q

INR

A

Normal:

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48
Q

Warfarin

A 
Anticoagulant
Mech:
   Inhibits synth & y-carboxylation of vit K dependent 
   clotting factors: VII, X, IX, II
Metabolized by CYP450 system (CYP2C9)
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49
Q

Griseofulvin

A

Tx: superficial fungal infections
DDI: CYP450 inducer

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50
Q

Erythromycin

A

Macrolide antibiotic

DDI: CYP450 antagonist

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51
Q

Isoniazid

A

Antibiotic
tx: TB
DDI: CYP450 inhibitor

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52
Q

Ketoconazole

A

Antifungal

DDI: CYP450 inhibitors (like all azoles)

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53
Q

Ritonavir

A

Protease inhibitor
Tx: HIV triple therapy
DDI: CYP450 inhibitor

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54
Q

Hypertrophic Cardiomyopathy

A

=hypertrophy w/asym septal enlargement w/o free wall enlargement
Asc:
-mut in myosin-binding protein C (AD)

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55
Q

Causes of Dilated CM

A
  • Enterovirus (coxsakie B)- myocarditis
  • Alcohol abuse
  • wet beriberi
  • cocaine
  • Chagas dz
  • doxorubicin toxicity
  • hemochromatosis
  • peripartum CM
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56
Q

Clonidine

A 
a2 receptor agonist
Side Effects:
  -depression, drowsy
  -Dry mouth
  -constipation
  -erectile dysfunction
  -disturbance of sleep cycle
  -confusion
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57
Q

Class IA Antiarrhythmics

A 
"Queen Proclaims Diso's pyramid"
Quinidine
Procainamide
Disopyramide
Mech: 
   ^: AP duration, refractory period, QT
Use: Atrial & ventricular arrhythmias
    *esp re-entrant & ectopic SVT & VT
Side Effects:
   Quinidine: cinchonism, dig tox
   Procainamide: SLE like syndrome
   Disopyramide:HF
   -HF
   -thrombocytopenia
   -Torsades de pointes
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58
Q

Class IB Antiarrhythmics

A 
"I'll Buy Liddy's Mexican Pinatas"
1B= Lidocaine, Mexiletine + Phenytoin
Mech:
  decrease AP duration
  Preferentially: ischemic or depolarized purkinje  & ventricular tissue
Use:
   -acuteventricular arrhythmias (esp post MI)
   -Dig induced
Side effects:
   -CNS stimulation/depression
   -CV depression
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59
Q

Class 1C AntiArrhythmics

A 
"Fries Please"
Flecainide
Propafenone
Mechs:
   slow phase 0, ^ refractory time in AV 
   No affect on AP
   No affect on refractory time in purkinje & ventricle
Tx:
   -SVT (Afib)
Adverse:
   -Proarrhythmic
   -NO for structural or ischemic heart dz (post MI)
60
Q

MI Markers

A 
Troponin I:
  -4 hrs -1wk
  -most specific
CK-MB (creatine-kinase myocardial bound)
   -increased for 6hrs-2 days
   -also in skeletal muscle
   -best for re-infarction
61
Q

Class I antiarrythmics

A

Decrease phase 0 slope, decrease conduction v
State dependent
IA/C: increase refractory period

62
Q

Antiarrhythmics: Increase refractory period

A

IA, IC (AV node only)

III

63
Q

Antiarrhythmics: decrease conduction velocity

A

I, III, amiodarone

64
Q

ENa
ECa
EK

A 
ENa= +25 (wants IN cell)
ECa= +124
EK= -90 (wants OUT of cell)
65
Q

Absolute Refractory Period
Effective Refractory Period
Relative Refractory period

A

Absolute Refractory Period:
=Phase0-after plateau: NO AP can initiate
Effective Refractory Period
=slightly longer than ARP
Phase0-right before Phase 3 ends
AP can’t be initiated by a local non-propagated
response can-only local (a few Na are open)
Relative Refratory Period
AP can be initiated but must be stonger
end tail of phase 3
*Determined by reactivation of Na channels that are inactivated after phase 0
*why don’t give electrical shock in relative refractory period!!

66
Q

Resting membrane potential of cardiac myocytes

A

-90 (Ek=-90)

67
Q

Cardiac AP Conduction pathway

A

Sa node –> atria –> AV node –> bundle of His –> R & L bundle branches –> purkinje fibers
–>Left bundle br–>L anterior & L post fasicles

68
Q

AV node blood supply

A

RCA

post. inf. interatrial septum

69
Q

Normal Sinus Rhythm

A

60-100 bpm
1,500/#small boxes
Large boxes: 300-150-100-75-60-50
=P precedes each QRS by normal PR (

70
Q

Sinus Arrhythmia

A

Normal
HR changes due to reflux changes in vagal tone during
respiration
Inspiration: decrease vagal tone –> ^ HR

71
Q

A-fib

A 
=regularly irregular heart beat
   -jagged baseline
   -no discrete P
   -irregular QRS intervals  (RRs don't match up)
RF:
  -hypertension
  -CAD
Complications:
   -thromboembolic --> stroke
        *LA dilated --> atrial clot
Tx:
  -anticoag
  -Rate control
  -Rhythm control
  -&/or cardioversion
72
Q

Atrial Flutter

A 
Sawtooth
  -indentical atrial depolarizations
  -even RR btwn QRS
Tx:
   //A-fib
        -anticoag
        -Rate control
        -Rhythm control
   Best: catheter ablation
73
Q

V-Fib

A

Completely erratic
Fatal
Tx:
CPR & defibrillation

74
Q

AV block: 1st degree

A

PR (>.2s, 4 boxes)

-benign

75
Q

AV Block: 2nd degree

Mobitz 1 & 2

A

Mobitz 1:
-increasing PR until P w/o QRS –> starts again
Mobitz 2:
-Constant PR, Some P w/QRS

76
Q

AV Block: 3rd degree

A

Complete block (his-purkinje)
Atria & ventricles beat independently
P-P constant
R-R cosntant, slower

77
Q

ANP (atrial natriuretic peptide)

A 
Atrial myocytes release ANP due to:
   ^Blood vol, atrial P
Causes:
  -Vasodilation
  -Causes diuresis
      -afferent arteriole: dilate
      -Efferent arteriole: constrict 
      -decrease Na reabsorption (& water too)
78
Q

BNP (B type natriuretic peptide)

A

From ventricular myocytes due to ^tension
//ANP but longer half-life
-Used for diagnosing HF
-Recombinant form (nesiritide): Tx HF

79
Q

What changes QT length

A

QT= ventricular contraction
^QT:
-prolonged Phase 3
-low Ca

80
Q

What changes PR

A

Normal PR:

81
Q

Delta on EKG

A

Wolf-Parkinson-White

82
Q

Aortic Arch baroreceptor action

A

Responds to BP –> vagus nerve (X) –> solitary nuc of medulla
^BP: ^ firing (parasymp)
Decreased BP: decrease firing –> symp takes over

83
Q

Carotid sinus Baroreceptor path

A

Carotid sinus –>glossopharyngeal n (IX)–>solitary nuc of medulla

84
Q

Peripheral Chemoreceptors

A

-Carotid & aortic bodies
Mediate changes in ventilation in response to:
-Low O2
-^CO2
-pH
1. Low O2 (altitude)
-doesn’t kick in until hypoxic drive to ^ventillation
2. ^Co2: fast, seconds
eg. climbing stairs
3. ^[H]:
-fast
-only mediator of response to metabolic acid/base
insults (ketoacidosis)
-bc metabolic doesn’t create CO2 to cross BBB

85
Q

Central Chemoreceptors

A

Ventral medulla
H+ can’t cross BBB
CO2 crosses –> special carbonic anhydrase converts
–> H+ binds H+ receptor (CSF has low buffer)
Slow response (minutes)
-day to day regulation
eg. bronchitis, pathological V/Q mismatch

86
Q

RA P

A
87
Q

RV P

A

25/5

88
Q

Pulm Artery P

A

25/10

89
Q

LA P

A
90
Q

LV P

A

130/10

91
Q

Aortic P

A

130/90

92
Q

Net fluid Flow (Jv)

A

Net Fluid Flow = Kf [(Pc-Pi) -c(oncoticc - oncotici)]
Kf: permeability of cap to fluid
C: permeability of cap to protein

93
Q

Edema Causes

A

^cap P: ^vol, HF
Decreased Plasma proteins:
-nephrotic, liver failure, malnurition
^Cap Permeability (Kf): toxin, infection, burn
^interstitial osmotic P: lymph blockage

94
Q

Causes of Torsades de Pointes

A

-Congenital long QT
-Hypokalemia
-hypomagnesemia
-hypocalcemia
-Diarrhea
-Alcoholism
ABCDE
Anti Arrhythmics
-Class IA anti-arrythmics
-Quinidine, Procainamide, Disopyramide
-Class IIII (except amiodarone)
-Ibutilide, Dofetilide, Sotalol
Anti-Biotics (macrolides)
Anti-Cytoics (haloperidol)
Anti-Depressants (TCAs)
Anti-Emetics (ondansetron)

95
Q

Strep Pyogenes

A 
2 autoimmune complications:
  i. Rheumatic Fever 
     Risk decreases w antibiotics
      -->rheumatic heart dz
         Rheumatic Heart dz causes:
              -mitral stenosis
             -Afib
  ii. Glomerulonephritis 
      **Risk does not decrease w antibiotics
      -immune complexes
96
Q

Libman-Sacks Endocarditis

A

=due to non-bacterial vegetations on both surfaces of mitral valve

  • may cause regurg
  • asc: SLE
97
Q

Non-bacterial Thrombotic endocarditis: Causes

A
  • libman-Sacks Endocarditis
  • Mucin producing adenocarcinoma
  • Hypercoagulative state
  • SLE
98
Q

Fetal shunts

A
  1. Ductus Venosus (–>ligamentum venosum)
    -bypass liver
    Umbilical v –>ductus venosus –>ICV
    2.Foramen Ovale (–>Fossa Ovalis)
    -bypass lungs
    -RA–>Formaen ovale –>LA
  2. Ductus Arteriosus (–>Ligamentum Arteriosum)
    -bypass lungs
    -Pulm a –>Ductus arteriosus –> desc aorta’
    -Keep PDA open: PGE1,2
    -Close PDA: Indomethacin
99
Q

AllaNtois becomes..

A

AllaNtois –>urachus –> mediaN umbilical lig

btwn blatter & umbillicus

100
Q

Notochord becomes…

A

nucleus pulposus

101
Q

UmbiLical arteries become…

A

MediaL umbilical ligaments

102
Q

Umbilical vein becomes…

A

Ligamentum Teres hepatis

w/in falciform ligament

103
Q

SA & AV nodes: Blood supply

A

R coronary artery

-MI causes bradycardia, heart block

104
Q

Dysphagia (difficulty swallowing) & hoarseness caused by:

A

compression of L recurrent laryngeal n (part of vagus)

105
Q

CO=

A

CO = SV x HR
CO= rate of O2 consumption (ml/min)/
arterial [O2] - venous [O2]
CO = MAP/SVR

Early exercise: CO maintained by ^HR & ^SV
Later exercise: CO maintained only by ^HR
^HR: shortens diastole

106
Q

^ Pulse Pressure (systolic P - diastolic P): Causes

A
  • Hyperthyroidism
  • Aortic Regurg
  • Aortic stiffening
  • Obstructive sleep apnea (^ symp tone)
  • Exercise (transient)
107
Q

Decreases Pulse Pressure (systolic P - diastolic P): Causes

A
  • Aortic Stenosis
  • Cardiogenic shock
  • Cardiac Tamponade
  • Advanced HF
108
Q

Aortic area: systolic Murmur

A
  • Aortic Stenosis

- Aortic valve sclerosis

109
Q

Pulmonic area: systolic ejection murmur

A
  • Pulmonic stenosis

- flow murmur

110
Q

Tricuspid area:

i. Holosystolic murmur
ii. Diastolic Murmur

A

i. Holosystolic murmur
- Tricuspid murmur
- VSD
ii. Diastolic Murmur
- Tricuspid stenosis
- ASD (^ flow across tricuspid valve)

111
Q

Mitral Area:

i. Holosystolic murmur
ii. Diastolic Murmur

A

i. Holosystolic Murmur
- Mitral regurg
ii. Diastolic Murmur
- Mitral stenosis

112
Q

Left Sternal Border

i. Systolic Murmur
ii. Diastolic Murmur

A

i. Systolic Murmur
- Hypertrophic CM
ii. Diastolic Murmur
- Aortic/pulmonic regurg

113
Q

Handgrip:

A 
^afterload
^: 
   Mitral regurg
   Aortic regurg
   VSD
Decrease:
   Hypertrophic CM ( equalizing pressures)
Mitral valve prolapse: later onset of click/murmur
114
Q

Inspiration PE for murmurs

A

^ venous return to RA

^: R heart sounds

115
Q

Valsalva Phase II, Standing up

A

Decrease preload
Decrease: most murmurs (including AS)
^:Hypertrophic CM: bc ^outflow obstruction w/low vol
MVP: later onset

116
Q

Rapid Squatting

A

^venous return, ^ preload, ^ afterload
Decrease: Hypertrophic CM
^AS
MVP: Later onset

117
Q

Drug Induced Long QT

A 
ABCDE
Antiarrhythmics (Ia, III)
AntiBiotics (macrolides)
Anti-"C"ychotics (haloperidol)
Anti-Depressants (TCAs)
Anti-Emetics (ondansetron)
118
Q

Primary HTN TX

A
  • Thiazide diuretics (decrease blood vol)
  • ACEi/ARBs (vasodilate, decrease blood vol)
  • Dipine CCB (vasodilate)
119
Q

HTN + HF TX

A
  • Diuretics (decrease vol)
  • ACEi/ARBs (decrease vol, vasodilate)
  • Aldo receptor antagonists (decrease vol)
  • B blockers** (decrease HR, ..)
    • *careful in decompensated HF
    • *NOT in cardiogenic shock
120
Q

HTN + DM Tx

A
  • ACEi/ARB
    • protects against diabetic neuropathy
  • CCB
  • Thiazide diuretics
  • B-blockers
121
Q

HTN in preg

A
  • Hydralazine
  • Labetalol
  • Methyldopa
  • Nifedipine
122
Q

Rheumatic Fever

A

Cause: Pharyngeal: B-hemolytic strep
Can lead to:
-Rheumatic heart dz (Mitral>aortic»»tricuspid)
-Aschoff bodies (granuloma w/giant cells)
-Anitschkow cells (large macros w wavy rod like nucs)
-^ASO titers (anti-streptolysin)
Jones Criteria:
-Joint (migratory polyarthritis)
-

123
Q

Pulsus Paradoxus

A 
-Decreased systolic BP >10 during inspiration 
In:
  -Cardiac tamponade
  -Asthma
  -Obstructive sleep apnea
  -pericarditis
  -Croup
124
Q

GERD vs MI

A

Both present as angina

  • GERD:
    • usually w/large meals
    • ^es when laying down
      - MI:
    • respiratory symps
    • neg cardiac enzymes
125
Q

Bupivacaine

A
  • local anesthetic
  • Amide based
  • cardiotoxic:
    • arrhythmias
    • Hypotension
126
Q

Normal WBC count

A

4,500-11,000 WBC/uL

127
Q

Normal Platelet Count

A

150,000-450,000 plats/uL

128
Q

Normal PCWP

A

PCWP = 4-12 mmHg

  • PCWP & CVP (central venous P) correlate with eachother
129
Q

Drugs that cause coronary vasospasm

A
  • Cocaine
  • Sumatriptan
  • Ergot Alkaloids
130
Q

Drugs that cause cutaneous flushing

A

VANCE

  • Vanco
  • Adenosine
  • Niacin
  • CCB
  • Echinocandins
131
Q

Norepinephrine: side effect

A 
Reflex Bradycardia:
Stimulate 
   a1: ^BV contract --> ^BP--> ^ venous return --> ^SV
   B1: ^inotrope, ^HR
CO= HR x SV
Can maintain CO  by decreasing HR
132
Q

alpha 1 receptor actions

A
  • BV contraction
  • Pupillary dilator m contraction (mydriasis)
  • Intenstinal & bladder sphincter m contraction
133
Q

alpha 2 receptor actions

A
  • Decrease
    • sympathetic outflow
    • insulin release
    • lipolysis
    • aqueous humor production
  • Increase:
    • plat aggregation
134
Q

B1 receptor actions

A 
Heart:
   Increase:
      -HR
      -contractility
Kidney: renin release
Increase Lipolysis
135
Q

Beta 2 receptor actions

A

-BV dilation
-bronchodilation
-lipolysis
-insulin release
-ciliary m. relaxation
-aqueous humor production
Decrease:
-Uterine tone (tocolysis)

136
Q

Beta 3 receptor actions

A
  • lipolysis

- thermogenesis in skeletal m

137
Q

Dopaminergic (D1) receptor actions

A

-renal BV dilation

138
Q

Dopaminergic (D2) receptor actions

A

-modulates transmitter release (esp brain)

139
Q

Histamine (H1) receptor actions

A
  • nasal/bronchial mucus production
  • BV permeability
  • bronchiole contraction
  • pruritus
  • pain
140
Q

Histamine (H2) receptor actions

A

-gastric acid secretion

141
Q

Muscarinic (M1) receptor actions

A
  • CNS

- enteric nervous system

142
Q

Muscarinic (M2) receptor actions

A
  • decrease HR

- decrease atria contractility

143
Q

Muscarinic (M3) receptor actions

A
  • exocrine gland secretions (lacrimal, seat, salivary, gastric)
  • gut peristalsis
  • bladder contraction
  • bronchoconstriction
  • pupillary sphincter m contraction (miosis)
  • ciliary m contraction (accomodation)
144
Q

Vasopressin (V1) receptor actions

A

-BV contraction

145
Q

Vasopressin (V2) receptor actions

A

-H2O permeability/reabsorption in collecting tubules

V2 is in the 2 kidneys

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