Brainscape's Knowledge GenomeTM

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


See full index

PANCE Practice > PANCE Prep- Cardiology Part 2 > Flashcards

PANCE Prep- Cardiology Part 2 Flashcards

1
Q

What creates S1, S2, S3, S4 and what disease are associated with them

A

S1- MV and TV closure (loudest at apex)
S2- AV and PV closure (loudest at base)
S3- rapid passive ventricular filling
-LVSF, normal in kids

S4- atrial contraction into the ventricles
-HTN, LVH, AS, normal in kids

Split S2: delayed PV closure

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

What murmurs radiate and to where?

A

AS- carotids
AR- LUSB
MS- none
MR- axilla

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

What positions increase murmur intensities?

What positions decrease murmur intensities?

A
  1. increase venous return increases ALL murmurs except HCM–> squatting, leg raise, lying down
  2. Right sided murmurs increase w/ inspiration
  3. Left sided murmurs increase w/ expiration
  4. Hand grips increases afterload–> increases regurg murmurs (AR and MR)
  5. decreasing venous returns decreases all murmurs except HCM–> valsalva, standing
  6. Amyl nitrate decreases afterload–> decreased regurg murmurs (AR and MR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Complications of AS

A

think AS Complications

  1. Angina (increased O2 demand but fixed CO due to obstructed LVoutlow
  2. Syncope w/ exertion
  3. CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Systolic ejection murmur, crescendo-decrescendo murmur heard at RUSB that radiates to carotids

  • pulsus parvus et tardus: small, delayed carotid pulse
  • Narrowed pulse pressure***
A

AS

DX: Echo, EKG: LVH

TX: surgery

  • no medical therapy is truly effective
  • AVOID physical exertion/venodilators (nitrates) neg. inotropes (CCB, BB)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

diastolic, decresendo, blowing murmur at LUSB

  • bounding pulses*
  • wide pulse pressure*
  • Hill’s sign: popliteal artery systolic pressure > brachial artery by 60mmHg
  • Water Hammer pulse- swift upstroke and rapid fall of radial pulse accentuated w/ wrist elevation
  • Corrigans pulse- similar to water hammer pulse but in referringto carotid artery
A

AR

DX: Echo

TX:

  1. surgery
  2. afterload reduction with vasodilators (ACEI, ARBs, Nifedipine, Hydralazine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

-Ruddy flushed cheeks with facial pallor
-dyspnea
-early-mid diastolic rumble at apex esp. in LLD position
-Prominent S1 and opening snap
+/- afib

A

MS MC caused by rheumatic heart disease by far

DX: echo, ekg- LAE +/- afib

TX: surgery

  1. meds-does not alter need for surgery
    - loop diuretics and Na restriction (if congestion)
    - BB, digoxin if Afib
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  • Dyspnea, +/- afib
  • blowing holosystolic murmur at apex w/ radiation to axilla
  • widely split S2
  • hyerdynamic LV on echo
A

MR *MC cause is MVP and ischemia

DX: echo

TX: surgery
2. meds- vasodilators to decrease afterload (ACEI, hydralazine) decrease preload (diuretics), digoxin if afib

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

MVP is usually asymptomatic but some may experience:

A

autonomic dysfunction: anxiety, atypical CP, palps–> then tx w/ BB but otherwise no tx is needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

harsh midsystolic ejection cresc-decrecendo murmur at LUSB radiates to neck
-systolic ejection click

A

PS *almost always congenital

TX: balloon valvuloplasty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

brief decrescendo early diastolic murmur at LUSB with full inspiration (Graham Steell murmur)

A

PR *almost always congenital

TX: none needed- well tolerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

mid-diastolic murmur heard at LLSB at 4th ICS

  • opening snap
  • can lead to RHF
A

TS

TX: surgery
2. meds- diuretics and na restriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

holosystolic blowing high pitched murmur at subxyphoid area (L mid sternal border)
-Carvallo signs- increased murmur intensity w/ inspiration

A

TR

TX: surgery
2. meds- diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q 
describe the pathophysiology of 
AS
MS
AR
MR
A

AS: LV outflow obstruction–> fixed CO
-increased afterload–> LVH
MS: Obstruction of flow from LA to LV–> increased LAE andLA pressure–> PHTN
AR: back flow from aorta to LV–> LV volume overload
MR: back flow from LV into LA–> LV volume overload–> decreased CO

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

common causes of secondary HTN

A

*consider if BP is refractory to antihypertensives or severly elevated

  1. Renovascular (MC): renal artery stenosis
  2. Fibromuscular dysplasia
  3. atherosclerosis
  4. Endocrine: primary hyperaldosteronism, PCC, Cushings
  5. Coarc, OSA, ETOH, OCPs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

__ is 2nd MC cause of ESRD is US

A

HTN

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

describe the different grades of retinopathy

A

I: arterial nicking
II: AV nicking
III: hemorrhages and soft exudates
IV: papilledema

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

what is the initial tx of choice for uncomplicated HTN

A

thiazide diuretics

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

SE of:

  1. Thiazide diuretics
  2. Loop diuretics
  3. K sparing diuretics
A
  1. Thiazide diuretics: HypoK+, HypoNa+, HyperCa++, Hyperglycemia, Hyperuricemia (caution w/ gout)
  2. Loop diuretics: HypoK+, HypoNa+, HypoCa++, metabolic akalosis, Ototoxicity,
    * CI: sulfa allergy
  3. K sparing diuretics: HyperK*, gynecomasia
    * CI: renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When is it best to use ACEI for HTN and what are their SE

A
  1. Hx of DM, nephropathy or CHF, post MI–> renoprotective**

SE:

  1. hypotension w/ first dose
  2. azotemia/RI
  3. HyperK+
  4. Cough/angioedema
  5. hyperuricemia
    * CI: pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the 2 types of CCBs?

A

Dihydropyridines: potent vasodilator w/ little or no effect on cardiac contractility or conduction
ex. Nifedipine and amlodipine

Non-dihydropyridines: affects cardiac contractility and conduction

  • used w/ HTN w/ concomitant Afib and used for raynauds
    ex. verapamil, diltiazem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

SE of CCBs

A

HA, dizziness, LH, flushing, peripheral edema,
Verapamil: constipation

CI: 2nd and 3rd Heart block, CHF

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

SE of BB

A

fatigue, depression, impotence, masked sympathetic sx of hypoglycemia (caution w/ diabetics)

  • may worsen PVD or raynauds
  • CI: 2/3 Heart block, asthma, decompensated HF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

good HTN med to use w/ BPH

A

A1 blockers
prazosin
terazosin
doxazosin

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

What antihypertensive med should you use to treat HTN w/ comorbid:

  1. afib
  2. angina
  3. post MI
  4. Systolic HF
  5. DM
  6. isolated HTN in elderly
  7. BPH
  8. AA
  9. Gout
A
  1. afib: BB or CCB
  2. angina: BB or CCB
  3. post MI: BB or ACEI
  4. Systolic HF: ACEI, ARB, BB, diuretic
  5. DM: ACEI
  6. isolated HTN in elderly: diuretic
  7. BPH: a1 blocker
  8. AA: thiazide, CCB
  9. Gout: CCB, Losartan (only ARB that doesn’t cause hyperuricemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Tx of Hypertensive Urgency

A

decrease BP by 25% over 24-48 hrs using oral meds
-clonidine or captopril

*Goal BP to = 160/100mmHg

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

Tx goals of hypertensive emergency

A

decrease BP by 25% in first hr then additional 5-15% over next 23 hrs using IV agents UNLESS:

  1. ischemic stroke: only lower if >/=185/110mmHg for tpa candidiates or if >/=220/120 for non candidates
  2. Aortic dissection: BP often reduced to 100-120 SBP w/in 20 min
28
Q

What meds should you use for HTN emergency w/ neurologic sx (HTN encephalopathy, heorrhagic stroke, or ischemic stroke)

A

Nicardipine or labetalol

29
Q

What meds should you use for HTN emergency w/ cardiovascular sx

  1. Aortic dissection:
  2. ACS:
  3. Acute HF:
A
  1. Aortic dissection: BB- esmolol, labetolol
  2. ACS: nitroglycerin, BB (esmolol, metoprolol)
  3. Acute HF: Nitroglycerin, furosemide
30
Q

Indication for statins

A
  1. 40-75y/o with DM 1 or 2
  2. 40-75y/o w/o CV risk factors but 7.5% or greater for having MI or CVA w/ in 10 yrs
  3. 21y/o or older w/ LDL 190 or higher
  4. s/s clinical atherosclerotic CV disease
31
Q

Best meds to:

  1. lower LDL
  2. Lower TG
  3. Increase HDL
A
  1. lower LDL: Statins
  2. Lower TG: Fibrates
  3. Increase HDL: Niacin
32
Q

what is the only med that is safe in pregnancy to help tx hyperlipidemia

A

Bile acid sequestrants
(cholestyramine, colestipol, colesevelam)
*may increase TGs

33
Q

what valve is MC affected in infective endocarditis

A

MV

**TV is most commonly affected for LV drug users

34
Q

MC organisms that cause endocardititis

A

SBE: strep viridan
ABE: staph aureus
IVDU: MRSA
Men w/ h/o GI/GU procedures: Enterococci

Others: HACEK organisms (gram neg) (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Klingella)

35
Q

s/s of endocarditis

A
  1. Fever
  2. ECG conduction abnormalites
  3. Janeway lesions: painless erythematous macules on palms and soles
  4. Roth spots: retinal hemorrhages w/ pale centers, Petechiae
  5. Osler nodes: tender nodules on pads of digits
  6. Splinter hemorrhages of prox. nail beds
36
Q

How do you dx Endocarditis

A
  1. Blood cultures: 3 sets at least 1 hr apart if pt is stable
  2. EKG (prone to arrhythmias)
  3. Echo/TEE
  4. CBC: leukocytosis, anemia: increased ESR/RF

MODIFIED DUKE CRITERIA
*2 major OR 1 major + 3 minor OR 5 minor

Major:

  1. 2+ blood cultures
    • echo
  3. new valvular regurg

Minor:

  1. Predisoping condition (abnormal valves, IVDU, indwelling cath)
  2. Fever
  3. Vascular and embolic phenomena: Janeway, septic arterial or pulm. emboli
  4. Immunologic phenomona: Osler nodes, Roth, + RF,
    • blood culture
    • echo (worsening of existing murmur)
37
Q

Empiric therapy for endocarditis for someone with:

  1. Acute (native valve)
  2. Subacute (native valve)
  3. Prosthetic valve
  4. Fungal
A
  1. Acute (native valve)- Nafcillin + Gentamicin or vanco + Gentamicin (if MRSA suspected)
  2. Subacute (native valve)- PCN or Ampicillin + Gentamicin (Vanco if IVDU)
  3. Prosthetic valve- Vanco+ Gentamicin + Rifampin (for s. aureus)
  4. Fungal- Amphotericin B
  • DURATION= 4-6 weeks
  • Gentamicin= gram neg coverage
  • PCN and Vanco= gram pos. coverage
38
Q

When is endocarditis prophylaxis indicated and what is it?

A
  1. Prosthetic (artificial) heart valve
  2. Hear repair using prosthetic material (nots stents)
  3. Hx of endocarditis
  4. Congenital Heart disease
  5. Cardiac valvulopathy in transplanted heart

Use: Amox. 2g 30-60min prior or Clindamycin 600mg if allergy

39
Q
  • LE pain/discomfort brought on by exercise or walking and relieved w/ rest
  • Claudication (buttock, thigh, calf)
  • Impotence
  • Decreased femoral pulses
  • atrophic skin changes, dusky red w/ dependency, lateral malleolar ulcers
A

PAD

DX:

  1. ABI: +PAD if ABI <0.90
  2. Arteriography (gold standard)
  3. hand held doppler- used in ED

TX: 1. Platelet inhibitor: Cilostazol mainstay of tx*, ASA, plavix

  1. Revascularization: PTA ,bypass, endarterectomy
  2. Supportive: exercise
40
Q

Where do AAA typically occur and what measurement is considered aneurismal

A

infrarenally

> 3.0cm (>5cm = increased risk of rupture)

41
Q

How do you dx AAA

A

DX: 1. Abdominal US- best initial test for suspected AAA and for monitoring progression in size

  1. CT: best for thoracic aneurysms and for further eval of known AAA
  2. Angiography- gold standard
42
Q

How do you treat AAAs

A
  1. 5.5cm or greater OR >0.5cm expansion in 6 months= immediate surgical repair even if asymptomatic
  2. > 4.5cm= vascular surgeon referal
  3. 4-4.5cm= monitor by US q6months
  4. 3-4cm= monitor by US q1yr

*BB reduces shearing forces and risk of rupture

43
Q

What is an aortic dissection and where is it is the worst place to have?

A

tear in the innermost layer of aorta (intima)

65% ascending= highest mortality

44
Q

What are risk factors of aortic dissections

A
  1. HTN
  2. age 50-60 (M>F)
  3. vasculitits
  4. collagen disorders
45
Q

Tx of aortic dissections

A

Surgical if: (A needs surgery ASAP)

  1. Acute proximal (Type A or I II)
  2. acute distal (type III) w/ complications

Medical management w/ esmolol., labetolol (SBP 100-120 and pulse <60) if:

  1. descending if no complications (B or III)
    * could use sodium nitroprusside added if needed
46
Q
  • superficial migratory thrombophlebitis
  • claudication/ distal extremity ischemia
  • raynauds phenomenon
  • STRONG ASSOCIATION W/ SMOKING
A

Thromboangiitis obliterans (Buerger’s disease)

DX: aortography- occlusive lesions of small and medium vessels- corkscrew collaterals (Gold standard)
2. abnormal Allen test (occlude radial and/or ulnar arteries)

TX:

  1. STOP smoking (only definitive management of Buerugers)
  2. Wound care
  3. CCB
47
Q

What is virchows triad

A

increased risk of PVD ( hypercoagulablility)

  1. Intimal damage
  2. stasis
  3. hypercoagulability (ex. FVL)
48
Q

what is the hypercoagulability work up?

A
  1. Factor V Leiden (MC)
  2. Prothrombin gene mutation
  3. Protein C and S def.
  4. Antiphospholipid Ab
  5. Lupus
  6. Factor VII def.
49
Q

How do you dx and tx DVT

A

DX: Venous duplex (1st line)

  1. d-dimer +/- Wells criteria
  2. Venography (gold standard)

TX:
1. Heparin (unfractionated heparin or LMWH (lovenox) –> Warfarin (overlap w/ heparin for at least 5 days)

50
Q

what is the MOA, duration of action, antidote, and SE of LMWH

A
  • MOA: potentiates antithrombin III
  • Duration of action: 12 hrs
  • Antidote: protamine sulfate
  • SE/CI: renal failure, thrombocytopenia
51
Q

what is the MOA, duration of action, antidote, and SE of unfractionated heparin

A
  • MOA: potentiates antithrombin III, inhibits thrombin and other coag. factors
  • Duration of action: 1hr
  • Antidote: protamine sulfate
  • SE: thrombocytopenia
52
Q
  • leg pain worse w/ prolonged standing/sitting, foot dependency
  • improves w/ elevation and walking
  • brownish hyperpigmentation
  • medial malleolus ulcer
  • pitting edema, stasis dermatitis
A

Chronic venous insufficiency

53
Q

How to measure orthostatic hypotension

A

2-5 min of quiet standing after a 5 minute period of being supine there is either:

  1. fall is SBP 20mmHg or more AND/OR
  2. fall in DBP 10mmHg or more
  • HR usually increases on standing- absence of increase is associated with autonomic dysfunction
  • increase in HR >15 may be due to hypovolemia
54
Q

Describe the 4 types of shock

A
  1. Hypovolemic: loss of blood or fluid volume (increase PVR and HR to maintain CO)
  2. Cardiogenic: primary myocardial dysfunction- reduced CO
  3. Obstructive: extrinisic or intrinsic obstruction to circulation (tamponade)
  4. distribution: maldistribution of blood flow from essential organs to nonessential organs
55
Q

Management of Shock

A 
ABC's
Airway
Breathing
Circulation
Delivery of oxygen
Endpoint resusication
56
Q
  • Pale, cool mottled skin
  • Prolonged capillary refill
  • Decreased skin turgor, dry mucous membranes
  • 2/2 hemorrhage, vomiting, diarrhea, severe burns
  • CO: decreased, PCWP: DECREASED, SVR: Increased
A

hypovolemic shock

57
Q
  • Severe respiratory distress
  • Cool clammy skin
  • 2/2 MI, myocarditis, valvular disease, cardiomyopathy, arrhythmia
  • -CO: decreased, PCWP: INCREASED, SVR: Increased
A

Cardiogenic shock

58
Q
  • Severe respiratory distress
  • Cool clammy skin
  • 2/2 tamponade, PE, tension pneumo, aortic dissection
  • CO: decreased, PCWP: INCREASED, SVR: Increased
A

Obstructive shock

59
Q

Describe the 4 types of Distributive shock

A
  1. Septic- severe host immune response- vasodilate
  2. Neurogenic- sympathetic blockade- unopposed vagal tone on vessels–> vasodilate
  3. Anaphylactic- IgE mediated HSN rxn w/ histamine release- vasodilation and cap. permeability
  4. Hypoadrenal- decreased corticosteroid and mineralocorticoid activity
60
Q
  • Increased CO***
  • Warm, flushed extremities and skin
  • Brisk cap refill
  • Bounding pulses, WIDE pulse pressure
A

Septic shock (only shock w/ increased CO)

61
Q

How do you treat hypovolemic shock

A
  1. ABCDEs
  2. volume resuscitation: crystalloids (NS or lactated ringer 3-4L)
  3. control hemorrhage source and prevent hypothermia
62
Q

How do you treat cardiogenic shock

A
  1. O2, isotonic fluids (avoid aggressive IV fluid tx- use smaller amounts of fluids*)– ONLY shock where large amounts of fluids are not given
  2. Inotropic support: dobutamine, epi
  3. tx underlying cause
63
Q

How do you treat obstructive shock

A
  1. O2, isotonic fluids, inotropic support: dobutamine, epi,

2. tx underlying cause

64
Q

How do you tx septic shock

A
  1. broad spectrum IV abx
  2. IV fluid resuscitation: NS or LR
  3. Vasopressors
65
Q

How do you tx anaphylactic shock

A
  1. Epi
  2. Airway managment
  3. Antihistamine (diphenhydramine or Ranitidine)
  4. IV fluids
  5. Observe patient for 4-6hrs
66
Q

how do you tx adrenal insufficiency (Addisonian crisis) shock?

A

Hydrocortisone 100mg IV

67
Q

What type of antibiotic interacts with statins and what does it increase the patients risk of?

A

statin + macrolides (clarithromycin)

*prolonged QT interval, myopathy and rhabdomyolysis

PANCE Practice (26 decks)

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