Cadiovasc NMBE Flashcards

1
Q

What are the types of large vessel vasculitis?

A

-Giant cell (temporal) Arteritis
-Takayasu Arteritis

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2
Q

How can you distinguish between the different large vessel vasculitis?

A

Giant cell
-“old women with jaw pain and vision loss”
-Unilateral headache
- Inc. ESR associated with polymyalgia rheumatica (joint and muscle pain/stiffness)
- Granulomatous thickening of carotids

Takayasu
-“young asian women with WEAK PULSES”
-Pulseless disease
-Granulomatous thickening of aortic arch

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3
Q

What are the types of medium vessel vasculitis?

A

-Polyarteritis Nodosa
-Kawasaki disease

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4
Q

What are some ways to distinguish medium vessel vasculitis?

A

Polyarteritis Nodosa
-PAN = HepB + renal prob + neuro prob
- Hepatitis B patient with renal and neuro problems
- SPARES lungs
- Fibrinoid necrosis–> String of pearls
-corticosteroids, cyclophosphamide

Kawasaki Disease
-CRASH and Burn;
-Conjunctivitis, Rash, Adenopathy (cervical), Strawberry tongue, Hand/foot edema, Burn (fever)
- Coronary vasculitis–> risk of aneurysm
- Aspirin and IVIG treatment

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5
Q

What kind of vasculitis is Buerger disease?

A

Medium vasculitis

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6
Q

Whats another word for buerger disease?

A

Thromboangiitis Obliterans

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7
Q

What are the types of small vessel vasculitis?

A

-Granulomatosis with polyangiitis
-Microscopic polyangiitis
-Eosinophilic granulomatosis with polyangiitis
- Henoch- Schönlein Purpura

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8
Q

Whats another name for granulomatosis with polyangiitis?

A

Wegeners disease

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9
Q

Whats another name for eosinophilic granulomatosis with polyangiitis?

A

Churg- Strauss

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10
Q

Whats another name for Henoch-Schonlein Purpura?

A

IgA vasculitis

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11
Q

What are some ways I can distinguish small vessel vasculitis?

A

Wegeners
-C-shaped symptoms
-C-ANCA
-C- shaped organs; nasopharynx, lungs, kidneys
-Hemoptysis, hematuria
-Necrotizing granulomas
-cyclophosphamide and steriods

Microscopic Polyangiitis
- Like wegeners but no granulomas or NO upper airway involvement
-P-ANCA
-cyclophosphamide and steriods

Churg-Strauss
-P-ANCA + eosinophilia
- History of asthma/allergies
-necrotizing granulomas
- cyclophosphamide and steroids

IgA Vasculitis
- IgA= Skin, GI, Kidneys
-PALPABLE purpura, arthritis, abdominal pain
-IgA nephropathy (hematuria)
-Often follows URI

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12
Q

What type of vasculitis present with recurrent oral and genital ulcers, uveitis and POSITIVE pathergy test?

A

Behcets syndrome

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13
Q

What are the main 4 types of shock

A

Cardiogenic Shock
Distributive shock
Hypovolemic shock
Obstructive shock

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14
Q

What is the main cause of cardiogenic shock?

A

Heart failure due to MI, arrhythmias, cardiomyopathy, valvular diseases (mitral regurg)

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15
Q

What is the pathophys of cardiogenic shock?

A

-Decreased CO due to pump failure
-increased afterload due to body compensating (RAAS and SNS)

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16
Q

What clinical features are associated with cardiogenic shock?

A

-Hypotension, tachy, cool extremities, pul. edema (dyspnea, crackles)
-JVD due to increased CVP (right atrial pressure)
-Low CO w/ high PCWP (due sucky ass left ventricle)
-increased TPR (body compensation)

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17
Q

What are the main causes of hypovolemic shock?

A

Decreased blood volume due to hemorrhage, fluid loss (vomitting, diarrhea, burns), or dehydration

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18
Q

What is the pathophys for hypovolemic shock?

A

-Decreased preload, leads to low CO
-Body compensates by activating RAAS, SNS, ADH secretion to preserve blood volume

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19
Q

What are the clinical features of hypovolemic shock?

A

-hypotension, tachy, cool extremities, reduced urine output
-Dry mucous membranes (dehydration)
-Low central venous pressure (CVP)
-Low PCWP

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20
Q

What are the big causes of distributive shock?

A

Systemic vasodilation due to…
-sepsis
-anaphylaxis
- neurogenic shock (spinal cord injury–> less SNS input)
-toxic shock syndrome

21
Q

What is the pathophysiology of distributive shock?

A

-MASSIVE vasodilation –> Decreased TPR—> shitty ass organ perfussion
-Decreased preload
-high/low CO depending on stage

22
Q

What are the clinical features of distributive shock?

A

-Warm skin (in sepsis and anaphylactic shock), due to vasodilation
-Hypotension
-Hyperdynamic circulation with bounding pulses (due to compensation) in sepsis and anaphylaxis
- Tachy
-elevated lactate levels (in septic shock due to tissue hypoxia)

23
Q

What are the main causes of obstructive shock?

A

Physical obstruction of blood flow due to PE, cardiac tamponade, tension pneumo

24
Q

What is the pathophys of obstructive shock?

A

-Decreased CO due to impaired blood flow
-increased afterload or pressure overload on the heart due to obstruction

25
Q

What are the clinical features of obstructive shock?

A

-hypotension, tachy, JVD (esp. in tamponade or tension pneumo)
-Sign of heart failure (dyspnea, pul. edema in tamponade)
-hypoxia, decreased breath sounds

26
Q

Which arteriolosclerosis is due to benign hypertension

A

Hyaline arteriolosclerosis

27
Q

Which arteriolosclerosis is due to malignant hypertension

A

Hyperplastic arteriolosclerosis

28
Q

What is the difference between malignant and benign hypertension?

A

Malignant- acute onset, causes organ damage off rip, medical emergency

Benign- happens overtime, takes time to cause damage to organs

29
Q

Pathophys for hyaline arteriolosclerosis

A

Benign hypertension and diabetes cause plasma proteins to leak into vessel wall causing narrowing of lumen and can cause renal failure

30
Q

pathophys for hyperplastic arteriolosclerosis

A

Malignant hypertension or arterioles causes smooth muscle proliferation to sustain all the tension, this results in thickening of the vessel (onion skin), which can potentially lead to end organ damage

  • renal failure, retinal hemorrhages, encephalopathy
31
Q

What is CVI

A

Venous valves of the lower legs are fucked with lead to retrograde flow and decreased venous blood to the heart

this leads to venous hypertension due to blood stasis

can lead to DVT

32
Q

What drugs are used for acute coronary syndrome

A

Anti-platelets

33
Q

MOA of aspirin

A

inhibits Cox-1—> decreased TXA2—> decreased platelet aggregation

34
Q

What is aspirin used for?

A

-Prevention of MI, stroke
-ACS
-Post stroke and MI

35
Q

Side effects of aspirin

A

Gastric ulcers, tinnitus, allergic rxn, renal injury, reye syndrome

36
Q

Which drugs have grel in their names

A

Clopidogrel
Ticagrelor
Prasugrel

37
Q

MOA of the grel drugs

A

Binds to ADP receptor (P2Y12), thus preventing ADP binding which decreases expression of GPIIb/IIIa

38
Q

What are the grel drugs used for

A

Combination with aspirin for ACU and PCI’s (stent placements)

39
Q

What are the side affects of the grel drugs

40
Q

What type of drug are the grel drugs

A

Anti-platelet drugs

41
Q

MOA for Abciximab

A

GpIIb/IIIa receptor inhibitor—> decreased platelet aggregation

42
Q

What is abciximab used for

A

ACS and during PCI

43
Q

Side effect for Abciximab, tirofiban, eptifibatide

A

Bleeding, thrombocytopenia, hypotension

44
Q

Which drugs block GpIIb/IIIa receptor?

A

abciximab, tirofiban, eptifibatide

45
Q

Which antiplatelet drugs have ol in their name

A

Cilostazol, dipyridamole

46
Q

MOA for dipyridamole, cilostazol

A

Blocks phosphodiesterase
–> increased cAMP
–> inhibition of platelet aggregation

47
Q

side effects for ol drugs

A

cilostazol, dipyridamole

headaches, hypotension, dizziness, nausea, abdominal pain

48
Q

what are cilostazol and dipyridamole used for

A

Claudication, stroke prevention, prevention of restenosis of stent