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Cardio > Cardiovascular Miscellany I > Flashcards

Cardiovascular Miscellany I Flashcards

1
Q

Cardiac Raynaud

A

coronary artery hyper-reactivity of sufficient duration (20-30 minutes)–can lead to variant angina

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2
Q

Prinzmetal angina

A

characterized by 5-15 minute episodes of angina pectoris AT REST (usually between midnight and early morning in association with ST-segment elevation)

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3
Q

What causes prinzmetal angina?

A

Vascular smooth muscle hyper-reactivity central to pathogenesis

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4
Q

Epidemiology of prinzmetal angina.

A

Japanese, <50 y/o, SMOKING (large risk factor)

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5
Q

Contraction Band Necrosis

A

transverse bands of hyper-contracted sarcomeres

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6
Q

What causes contraction band necrosis?

A

When cardiac myocytes run out of energy and are exposed to calcium, actin-myosin interactions are enhanced resulting in hypercontraction or a agonal titanic state of un-relaxable sarcomeres

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7
Q

In what 2 situations do you see contraction band necrosis?

A

May be due to repurfusion of dead myocardium or coronary artery vasospasm

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8
Q

What is another name for Takotsubo cardiomyopathy?

A

“broken heart syndrome”

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9
Q

Takotsubo cardiomyopathy

A

Coronary artery vasospasm due to emotional stress that can cause myocardial ischemia, MI, or sudden cardiac death.

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10
Q

Stasis Dermatitis

A

Erythematous, scaling, and eczematous patches or plaques affecting the lower extremities (meidal ankle most commonly involved) due to persistent edema from incompetent varicose vein valves

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11
Q

Varicose Ulcers

A

secondary ischemic skin ulceration due to persistent edema from incompetent varicose vein valves that had poor wound healing and superimposed infection

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12
Q

Esophageal Varices

A

liver cirrhosis leading to portal vein hypertension opens the porto-systemic shunts and increases blood flow into veins at the gatro-esophageal junction.

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13
Q

Caput medusae

A

liver cirrhosis leading to portal vein hypertension leads to increased blood flow into periumbilical veins of the abdominal wall

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14
Q

Hemorrhoids

A

increased blood flow to anorectal junction that results from prolonged pelvic vascular congestion associate with pregnancy or straining to defecate

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15
Q

Trosseau syndrome

A

venous thrombi may result from elaboration of procoagulant factors from malignant tumors—causing a hypercoagulable state that can manifest as evanescent thromboses in different vascular beds at different times

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16
Q

What is the most important risk factor for DVT?

A

Prolonged immobilizaiton leading to venous stasis is most important risk factor

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17
Q

Epidemiology of DVT.

A

COMMON 400,000/year, higher in men, increase with age

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18
Q

DVT is associated with what?

A

Can be associated with cancer (hypercoagulable state), hospitalization, surgery, and major trauma

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19
Q

Where do pulmonary emboli come from?

A

proximal thrombosis which is above popliteal vein

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20
Q

Diagnostics of DVT.

A

erythemia (SP), superficial venous dilation (SP), calf/ankle swelling (SN), swelling of entire leg (SP)

D-dimer is one of the best tests!

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21
Q

Homan sign.

A

pain in the calf on forceful and abrupt dorsiflexion of the patient’s foot at the ankle while the knee is extended (BAD test for DVT- you can dislodge thrombus)

22
Q

What neoplasms commonly lead to SVC syndrome.

A

bronchogenic carcinoma or mediastinal lymphoma

23
Q

Symptoms of SVC syndrome.

A

o Obstruction produces clinical complex of marked dilation of veins of head, neck, and arms (associated with cyanosis)
o Pulmonary vessels can be compressed—leading to respiratory distress

24
Q

What neoplasms commonly lead to IVC syndrome.

A

hepatocellular carcinoma and renal cell carcinoma

25
Q

Symptoms of IVC syndrome.

A

Marked lower extremity edema, distention of superficial collateral veins of lower abdomen, and marked proteinuria (with renal vein involvement)

26
Q

Chylothorax

A

rupture of dilated lymphatics followed by obstruction of infiltrating tumor mass that leads to milky accumulation of lymph in thoracic cavity

27
Q

Sturge-Weber Syndrome

A

Large facial telangiectasia in child with mental deficiency!

28
Q

What is another name for Osler-Weber-Rendu disease?

A

Hereditary Hemorrhagic Telangiectasis

29
Q

Osler-Weber-Rendu disease

A

autosomal dominant disorder caused by mutations in genes that encode components of the TGF-beta signaling pathway in endothelial cells.

30
Q

What are Telangiectasias composed of?

A

dilated capillaries and veins that are present at birth

31
Q

Where are the lesions and what are the symptoms of Osler- Weber-Rendu disease?

A

o Lesions present over skin and oral mucous membranes (as well as respiratory, GI and urinary tracts)
o Lesions spontaneously rupture causing nosebleeds, GI bleeds, and hematuria

32
Q

Hemangioma

A

very common tumors composed of blood filled vessels that regress spontaneously

33
Q

What is unique about Hemangiomas at touch?

A

they blanch!

34
Q

Pyogenic granuloma

A

capillary hemangiomas that manifest as rapidly growing red pedunculated lesions on the skin, gingival or oral mucosa.

35
Q

Lymphangioma

A

benign, lymphatic counterpart of hemangiomas

36
Q

Bacillary Angiomatosis

A

vascular proliferation in immunocompromised hosts caused by gram-negative bacilli of Bartonella family (ex. cat scratch disease and “trench fever” from lice)

37
Q

What is the pathogenesis of bacillary angiomatosis?

A

Bacteria induce host tissues to produce HIF-1alpha which stimulates VEGF production and vascular proliferation

38
Q

Pathology of bacillary angiomatosis.

A

o Skin lesions= red papules and nodules

o Infiltrating neutrophils, nuclear debris, purplish granular collections of causative bacteria.

39
Q

What virus is related to Kaposi Sarcoma? How?

A

HHV-8 (virally encoded G protein induces VEGF production, viral homologue of cyclin D drives proliferation, and KSHV-encoded protein inhibits p53)

40
Q

In what group of individuals is Kaposi Sarcoma very common? How can you treat them?

A

VERY common in AIDS patients (immunosuppressed)- involves lymph nodes and disseminates widely to viscera early in course. Can treat with HIV antiretroviral therapy or interferon-gamma and angiogenesis inhibitors

41
Q

Who gets Classical KS?

A

older men of Mediaterranean descent with malignancy or altered immunity.

42
Q

What do lesions of KS look like?

A
  • Multiple purple-red skin plaques or nodules (lower extremities)
  • Largely restricted to surface of body and surgical resection handles it
43
Q

Who gets endemic African KS?

A

younger (<40) HIV-seronegative patients; involves lymph nodes (MOST COMMON tumor in central Africa)

44
Q

Transplantation-Induced KS

A

solid organ transplant recipients with T cell immunosuppression can get KS in lymph nodes, mucosa, viscera, and absent cutaneous lesions

45
Q

Where are common sites of Kaposi Sarcoma?

A

ears, nose, toes/feet, penis

46
Q

What is angiosarcoma?

A

malignant endothelial neoplasms (aggressive and metastasizing) that often involve skin, soft tissue, breast and liver

47
Q

Hepatic angiosarcomas are associated with exposure to what?

A

PVC, arsenical pesticides

48
Q

Morphology of hepatic angiosarcoma

A

Small, sharply demarcated red nodules that progress to fleshy, large red-tan to gray-white masses with common necrosis and hemorrhage

49
Q

What is a stent?

A

tube put inside some tubular structure inside the body to keep it open

50
Q

What causes myocardial vessel vasospasm?

A

exogenous chemical use like cocaine/phenylephrine; people in extreme phychological stress; hyperthyroidism; scleroderma

51
Q

How do people with PE die?

A

right sided heart dilation and failure

Cardio (24 decks)

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