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
Symptoms of IVC syndrome.
Marked lower extremity edema, distention of superficial collateral veins of lower abdomen, and marked proteinuria (with renal vein involvement)
26
Chylothorax
rupture of dilated lymphatics followed by obstruction of infiltrating tumor mass that leads to milky accumulation of lymph in thoracic cavity
27
Sturge-Weber Syndrome
Large facial telangiectasia in child with mental deficiency!
28
What is another name for Osler-Weber-Rendu disease?
Hereditary Hemorrhagic Telangiectasis
29
Osler-Weber-Rendu disease
autosomal dominant disorder caused by mutations in genes that encode components of the TGF-beta signaling pathway in endothelial cells.
30
What are Telangiectasias composed of?
dilated capillaries and veins that are present at birth
31
Where are the lesions and what are the symptoms of Osler- Weber-Rendu disease?
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
Hemangioma
very common tumors composed of blood filled vessels that regress spontaneously
33
What is unique about Hemangiomas at touch?
they blanch!
34
Pyogenic granuloma
capillary hemangiomas that manifest as rapidly growing red pedunculated lesions on the skin, gingival or oral mucosa.
35
Lymphangioma
benign, lymphatic counterpart of hemangiomas
36
Bacillary Angiomatosis
vascular proliferation in immunocompromised hosts caused by gram-negative bacilli of Bartonella family (ex. cat scratch disease and “trench fever” from lice)
37
What is the pathogenesis of bacillary angiomatosis?
Bacteria induce host tissues to produce HIF-1alpha which stimulates VEGF production and vascular proliferation
38
Pathology of bacillary angiomatosis.
o Skin lesions= red papules and nodules | o Infiltrating neutrophils, nuclear debris, purplish granular collections of causative bacteria.
39
What virus is related to Kaposi Sarcoma? How?
HHV-8 (virally encoded G protein induces VEGF production, viral homologue of cyclin D drives proliferation, and KSHV-encoded protein inhibits p53)
40
In what group of individuals is Kaposi Sarcoma very common? How can you treat them?
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
Who gets Classical KS?
older men of Mediaterranean descent with malignancy or altered immunity.
42
What do lesions of KS look like?
* Multiple purple-red skin plaques or nodules (lower extremities) * Largely restricted to surface of body and surgical resection handles it
43
Who gets endemic African KS?
younger (<40) HIV-seronegative patients; involves lymph nodes (MOST COMMON tumor in central Africa)
44
Transplantation-Induced KS
solid organ transplant recipients with T cell immunosuppression can get KS in lymph nodes, mucosa, viscera, and absent cutaneous lesions
45
Where are common sites of Kaposi Sarcoma?
ears, nose, toes/feet, penis
46
What is angiosarcoma?
malignant endothelial neoplasms (aggressive and metastasizing) that often involve skin, soft tissue, breast and liver
47
Hepatic angiosarcomas are associated with exposure to what?
PVC, arsenical pesticides
48
Morphology of hepatic angiosarcoma
Small, sharply demarcated red nodules that progress to fleshy, large red-tan to gray-white masses with common necrosis and hemorrhage
49
What is a stent?
tube put inside some tubular structure inside the body to keep it open
50
What causes myocardial vessel vasospasm?
exogenous chemical use like cocaine/phenylephrine; people in extreme phychological stress; hyperthyroidism; scleroderma
51
How do people with PE die?
right sided heart dilation and failure