All Block 1 materials (overview from cardiovascular-pulmonary)

Question 1

When the mucosa becomes inflamed & swollen (edematous) causing it to protrude

Usually caused by recurrent bouts of rhinitis

Associated with:
Cystic fibrosis
Aspirin-tolerant asthma

Describes which condition?

Answer 1

Nasal polyps

Question 2

A subset of rhinitis cause by a type I hypersensitivity reaction. It has inflammatory infiltrated with lots of eosinophils

Associated with:
Asthma
Eczema
Churg-Strauss vasculitis

Describes which condition?

Answer 2

Allergic rhinitis

Question 3

Describe what Rhinitis is, how it presents, & what the most common cause of it is

Answer 3

When the nasal mucosa becomes inflamed, usually due to the rhinovirus

Signs: Sneezing, Congestion, Runny nose/coughing

Question 4

Explain what allergic rhinitis is? What conditions is it associated with?

Answer 4

A subset of rhinitis cause by a type I hypersensitivity reaction. It has inflammatory infiltrated with lots of eosinophils

Associated with:
Asthma
Eczema
Churg-Strauss vasculitis

Question 5

Describe what a nasal polyp is?

What causes it?
What conditions is it associated with?

Answer 5

When the mucosa becomes inflamed & swollen (edematous) causing it to protrude

Usually caused by recurrent bouts of rhinitis

Associated with:
Cystic fibrosis
Aspirin-tolerant asthma

Question 6

Describe the following for Takayasu’s disease:

What is the pathophysiology?

What are the symptoms?

What artery is most likely affected?

Answer 6

Patho: aka pulseless disease

A large vessel vasculitis with granulomatous inflammation & giant cells that cause thickening & stenosis of the branching arteries of the aorta (type IV reaction usually in Asian ladies under 50yrs)

Symptoms:
1) Weak/absent pulse in the upper extremities
2) Differences between BP in upper vs lower ext
3) Syncope/dizziness
4) Paresthesia

Artery most affected: Subclavian A

Question 7

Patho: aka pulseless disease

A large vessel vasculitis with granulomatous inflammation & giant cells that cause thickening & stenosis of the branching arteries of the aorta (type IV reaction usually in Asian ladies under 50yrs)

Symptoms:
1) Weak/absent pulse in the upper extremities
2) Differences between BP in upper vs lower ext
3) Syncope/dizziness
4) Paresthesia

Artery most affected: Subclavian A

Describes which condition?

Answer 7

Takayasu’s disease

Question 8

Describe the following for Wegener’s granulomatosis:

What is the Pathophysiology?

What are the symptoms?

What are the lab findings?

What is a sequelae?

What is the treatment & the risk of no treatment?

Answer 8

Patho:
Body forms antibodies against proteinase-3 (PR3-ANCA aka P-ANCA) which cause necrotizing granulomas with giant cells & vasculitis in the upper & lower respiratory tract & in the kidneys

Symptoms:
1) Saddle nose deformity (Septum is destroyed by granulomatous inflammation)
2) Chronic sinusitis
3) Nasal ulcers
4) Granulomas in the upper & lower respiratory tracts
5) Pneumonia with nodular lesions
6) Hemoptysis
7) Renal disease (granulomatous inflammation)

Labs:
C-ANCA +ve
Bilateral nodular infiltrates

Sequelae:
Crescentic glomerulonephritis

Rx: Cyclophosphamide (risk Hemorrhagic cystitis & Transitional cell cancer)

Untreated results in an 80% death rate within the year

Question 9

Patho:
Body forms antibodies against proteinase-3 (PR3-ANCA aka P-ANCA) which cause necrotizing granulomas with giant cells & vasculitis in the upper & lower respiratory tract & in the kidneys

Symptoms:
1) Saddle nose deformity (Septum is destroyed by granulomatous inflammation)
2) Chronic sinusitis
3) Nasal ulcers
4) Granulomas in the upper & lower respiratory tracts
5) Pneumonia with nodular lesions
6) Hemoptysis
7) Renal disease (granulomatous inflammation)

Labs:
C-ANCA +ve
Bilateral nodular infiltrates

Sequelae:
Crescentic glomerulonephritis

Rx: Cyclophosphamide (risk Hemorrhagic cystitis & Transitional cell cancer)

Untreated results in an 80% death rate within the year

Describes which condition?

Answer 9

Wegener’s granulomatosis

Question 10

Describe the following for microscopic polyangiitis:

What is the pathophysiology?

What are the symptoms?

What is a key lab finding?

What is the treatment?

Answer 10

Patho:
Inflammation that only targets the lungs & kidneys

Symptoms:
1) Hypertension
2) Glomerular nephritis
3) Hemoptysis
4) Palpable purpura

Labs:
P-ANCA +ve

Rx:
Corticosteroids & Cyclophosphamide

Question 11

Patho:
Inflammation that only targets the lungs & kidneys

Symptoms:
1) Hypertension
2) Glomerular nephritis
3) Hemoptysis
4) Palpable purpura

Labs:
P-ANCA +ve

Rx:
Corticosteroids & Cyclophosphamide

Describes which condition?

Answer 11

microscopic polyangiitis

Question 12

Describe the following for Cryoglobulinemia:

What is the pathophysiology?

What are the symptoms?

What are the lab findings?

Answer 12

Patho:
Vasculitis triggered by a prior Hep C infection

Symptoms:
1) Hematuria
2) Palpable purpura
3) Arthralgia

Labs:
Hep C & Cryoglobulin deposits

Question 13

Patho:
Vasculitis triggered by a prior Hep C infection

Symptoms:
1) Hematuria/Glomerular nephritis
2) Palpable purpura
3) Arthralgia

Labs:
Hep C & Cryoglobulin deposits (IgG & IgM)

Describes which condition?

Answer 13

Cyroglobulinemia

Question 14

Describe the following for Kawasaki disease:

What is the pathophysiology?

What are the symptoms?

What are the lab findings?

What is a major sequelae concern?

What is the treatment?

Answer 14

Patho:
A childhood vasculitis affecting <4yr olds (Asian/Hawaiian) that involves transmural inflammation of the blood vessels from neutrophils & fibrinoid necrosis that result in coronary artery thrombosis or aneurysm.

Symptoms:
1) Conjunctivitis
2) Strawberry tongue
3) Erythematous rash (trunk/extremities)
4) Localized cervical lymphadenopathy
5) Edema
6) Fever
7) Desquamating skin

Labs:
ST Elevation
Thrombocytosis
Neutrophilic leukocytosis
Elevated ESR

Sequelae concern: MI in kids!!!!

Rx.
Aspirin with IV immunoglobulins

Question 15

Patho:
A childhood vasculitis affecting <4yr olds (Asian/Hawaiian) that involves transmural inflammation of the blood vessels from neutrophils & fibrinoid necrosis that result in coronary artery thrombosis or aneurysm.

Symptoms:
1) Conjunctivitis
2) Strawberry tongue
3) Erythematous rash (trunk/extremities)
4) Localized cervical lymphadenopathy
5) Edema
6) Fever
7) Desquamating skin

Labs:
ST Elevation
Thrombocytosis
Neutrophilic leukocytosis
Elevated ESR

Sequelae concern: MI in kids!!!!

Rx.
Aspirin with IV immunoglobulins

Describes which condition?

Answer 15

Kawasaki disease

Question 16

Describe the following for Churg-Strauss syndrome:

What is the pathophysiology?

What are the symptoms?

What are the lab findings?

What is the treatment?

Answer 16

Patho:
A systemic vasculitis that happens in patients with asthma or allergic rhinitis causing inflammation with eosinophilia, fibrinoid necrosis, & thrombosis in blood vessel walls

Symptoms:
1) Asthma/Allergic rhinitis
2) Eosinophilia

Labs:
P-ANCA +ve
IgE elevation
Eosinophilia
Thrombosis
Fibrinoid necrosis

Rx:
Corticosteroids

Question 17

Patho:
A systemic vasculitis that happens in patients with asthma or allergic rhinitis causing inflammation with eosinophilia, fibrinoid necrosis, & thrombosis in blood vessel walls

Symptoms:
1) Asthma/Allergic rhinitis
2) Eosinophilia

Labs:
P-ANCA +ve
IgE elevation
Eosinophilia
Thrombosis
Fibrinoid necrosis

Rx:
Corticosteroids

Describes which condition?

Answer 17

Churg-Strauss Syndrome

Question 18

Describe the following for Polyarteritis Nodosa:

What is the pathophysiology?

What are the symptoms?

What are the lab findings?

What are the concerning sequelae?

What is the treatment?

What is the main COD?

Answer 18

Patho:
Segmental transmural inflammation of the blood vessel that causes focal necrosis resulting in nodules & dilations. There is a strong association to HBV infection. This condition spares the lungs

Symptoms:
1) Hypertension
2) Hematuria (RBC casts)
3) Albuminemia
4) Abdominal pain & Melena (Mesenteric artery)
5) Skin ulcers & nodules

Labs:
HBsAg +ve (in 30% of cases)
RBC casts in urine
String of pears app on CT

Sequelae:
MI & Aneurysm

Rx:
Corticosteroids & Cyclophosphamide (risk HC & TCC)

Main COD:
Renal failure

Question 19

Patho:
Segmental transmural inflammation of the blood vessel that causes focal necrosis resulting in nodules & dilations. There is a strong association to HBV infection. This condition spares the lungs

Symptoms:
1) Hypertension
2) Hematuria (RBC casts)
3) Albuminemia
4) Abdominal pain & Melena (Mesenteric artery)
5) Skin ulcers & nodules

Labs:
HBsAg +ve (in 30% of cases)
RBC casts in urine
String of pears app on CT

Sequelae:
MI & Aneurysm

Rx:
Corticosteroids & Cyclophosphamide (risk HC & TCC)

Main COD:
Renal failure

Describes which condition?

Answer 19

Polyarteritis Nodosa

Question 20

Describe the following for Giant cell (Temporal) Arteritis:

What is the pathophysiology?

What are the symptoms?

What are the lab findings?

What is the treatment?

What is a risk of no treatment?

Answer 20

Patho:
Granulomatous inflammation with giant cells infiltrating the walls of blood vessels causing intimal fibrosis & segmented lesions.

Symptoms:
1) Protruding temporal artery
2) Severe headache (Temporal A)
3) Visual disturbances (Opthalmic A)
4) Jaw claudication
5) Arthralgia & flu-like signs

Labs:
Elevated ESR
Granulomatous inflammation with giant cells (Segmental lesions = segmental biopsy 60% +ve cases).

Rx:
Corticosteroids

Untreated risk:
Permanent blindness

Question 21

Patho:
Granulomatous inflammation with giant cells infiltrating the walls of blood vessels causing intimal fibrosis & segmented lesions.

Symptoms:
1) Protruding temporal artery
2) Severe headache (Temporal A)
3) Visual disturbances (Opthalmic A)
4) Jaw claudication
5) Arthralgia & flu-like signs

Labs:
Elevated ESR
Granulomatous inflammation with giant cells (Segmental lesions = segmental biopsy 60% +ve cases).

Rx:
Corticosteroids

Untreated risk:
Permanent blindness

Describes which condition?

Answer 21

Giant cell (temporal) arteritis

Question 22

Describe the following for Henoch-Schönlein Purpura:

What is the pathophysiology?

What are the symptoms?

What are the lab findings?

What is the treatment?

Answer 22

Patho: aka hypersensitivity leukocytoclastic vasculitis

An IgA immune mediated type III hypersensitivity resulting in immune complexes being deposited in tissues which activate compliments (C5a) to attract neutrophils causing ischemia with leukocytoclastic neutrophils. Usually right after a GI or Resp infection (B19 or S.aureus)

Symptoms:
1) Palpable purpura
2) Colicky abdominal pain
3) Hemoptysis
4) Hematuria with RBC casts
5) Arthralgia

Labs:
Leukocytoclastic neutrophils (fragmented)
RBC extravasation
Lots of fibrin (around BV)
IgA-C3 deposits

Rx: Remove the trigger (drug/food etc)

Question 23

Patho: aka hypersensitivity leukocytoclastic vasculitis

An IgA immune mediated type III hypersensitivity resulting in immune complexes being deposited in tissues which activate compliments (C5a) to attract neutrophils causing ischemia with leukocytoclastic neutrophils. Usually right after a GI or Resp infection (B19 or S.aureus)

Symptoms:
1) Palpable purpura
2) Colicky abdominal pain
3) Hemoptysis
4) Hematuria with RBC casts
5) Arthralgia

Labs:
Leukocytoclastic neutrophils (fragmented)
RBC extravasation
Lots of fibrin (around BV)
IgA-C3 deposits

Rx: Remove the trigger (drug/food, etc)

Describes which condition?

Answer 23

Henoch-Schönlein Purpura

Question 24

Describe the following for thromboangitis obliterans:

What is the pathophysiology?

What are the symptoms?
-early
-late

What is the treatment?

Answer 24

Patho: Buegers disease
Heavy smoking leads to acute inflammation causing obliteration of the lumen resulting in segmental thromboses of distal blood vessels & involves the entire neurovascular compartment.

Symptoms:
Early
1) Claudication of hands/feet
2) Muscle cramps (relieved by rest)
Late
3) Painful ulceration of digits
4) Necrosis & autoamputation of digits

Rx:
Smoking cessation

Question 25

Patho: Buegers disease Heavy smoking leads to acute inflammation causing obliteration of the lumen resulting in segmental thromboses of distal blood vessels & involves the entire neurovascular compartment. Symptoms: Early 1) Claudication of hands/feet 2) Muscle cramps (relieved by rest) Late 3) Painful ulceration of digits 4) Necrosis & autoamputation of digits Rx: Smoking cessation Describes which condition?

Answer 25

Thromboangitis obliterans

Question 26

Describe the following for atherosclerosis: What is the Pathophysiology (how it forms)? What conditions can it cause? What are the risk factors? -modifiable -non-modifiable

Answer 26

Patho: 1) damaged endothelium leaks lipids into the intima 2) Lipids are oxidized & eaten by macrophages turning them into foam cells (Fatty streaks) 3) The inflammation & healing due to the damage leads to deposition of ECM & proliferation of smooth muscle which trap the foam cells forming plaques Associated conditions: Risk factors

Question 27

Describe the following for arteriosclerosis: What is the pathophysiology? What are the two subtypes? What are the complications of the subtypes?

Answer 27

Patho: Thickening of the arteries due to protein deposition & smooth muscle cell proliferation in the arteries. Subtypes: Hyaline: Can be caused by benign hypertension (increased pressure pushes proteins into the BV wall) OR diabetes (non-enzymatic glycosylation of proteins makes them more permeable to leak into BV) Hyperplastic: Caused by malignant hypertension resulting in smooth muscle cell proliferation giving it an onion skin appearance Complications: 1) Renal failure with a flea bite appearance (HYPERPLASTIC) 2) Glomerular scarring aka arteriolonephrosclerosis (progresses to renal failure HYALINE)

Question 28

Patho: Thickening of the arteries due to protein deposition & smooth muscle cell proliferation in the arteries. Subtypes: Hyaline: Can be caused by benign hypertension (increased pressure pushes proteins into the BV wall) OR diabetes (non-enzymatic glycosylation of proteins makes them more permeable to leak into BV) Hyperplastic: Caused by malignant hypertension resulting in smooth muscle cell proliferation giving it an onion skin appearance Complications: 1) Renal failure with a flea bite appearance (HYPERPLASTIC) 2) Glomerular scarring aka arteriolonephrosclerosis (progresses to renal failure HYALINE) Describes what condition?

Answer 28

Arteriosclerosis

Question 29

Can be caused by benign hypertension (increased pressure pushes proteins into the BV wall) OR diabetes (non-enzymatic glycosylation of proteins makes them more permeable to leak into BV) Describes which condition?

Answer 29

Hyaline Arteriosclerosis

Question 30

Describe the pathophysiology of Hyaline arteriosclerosis

Answer 30

Can be caused by benign hypertension (increased pressure pushes proteins into the BV wall) OR diabetes (non-enzymatic glycosylation of proteins makes them more permeable to leak into BV)

Question 31

Caused by malignant hypertension resulting in smooth muscle cell proliferation giving it an onion skin appearance Describes which condition?

Answer 31

Hyperplastic arteriosclerosis

Question 32

Describe the pathophysiology of hyperplastic arteriosclerosis

Answer 32

Caused by malignant hypertension resulting in smooth muscle cell proliferation giving it an onion skin appearance

Question 33

What are the main arteries impacted by atherosclerosis?

Answer 33

** Abdominal aorta Coronary arteries Popliteal arteries Descending thoracic aorta Internal carotid artery

Question 34

Describe what Monkenberg-medial-calcification is?

Answer 34

It's non-obstructive calcification of the media that is NOT clinically significant

Question 35

It's non-obstructive calcification of the media that is NOT clinically significant

Answer 35

Monkenberg-medial-calcification

Question 36

Describe the following for Aortic Dissection: What is the pathophysiology? - Two major causes What are the symptoms? What are the complications?

Answer 36

Patho: 1) In older patients, HTN causes hyaline arteriosclerosis of the vaso vasorum resulting in media atrophy & weakness which leads to an intimal tear 2) In younger patients, there is usually an inherited CT disorder (Marfans/EDS) that result in cyctic medial necrosis resulting in wall weakness & an intimal tear Symptoms: 1) Sharp tearing chest pain radiating to the back 2) Hypertension 3) Widened mediastinum 4) Syncope Complications: Pericardiac tamponade (MCOD)

Question 37

Patho: 1) In older patients, HTN causes hyaline arteriosclerosis of the vaso vasorum resulting in media atrophy & weakness which leads to an intimal tear 2) In younger patients, there is usually an inherited CT disorder (Marfans/EDS) that result in cyctic medial necrosis resulting in wall weakness & an intimal tear Symptoms: 1) Sharp tearing chest pain radiating to the back 2) Hypertension 3) Widened mediastinum 4) Syncope Complications: Pericardiac tamponade (MCOD) Describes which condition?

Answer 37

Aortic dissection

Question 38

Describe the following for a Thoracic aneurysm: What is the pathophysiology? - Two major causes What are the symptoms? What are the complications?

Answer 38

Patho: 1) Atherosclerosis causes HTN which results in atrophy of the media causing a ballooning aneurysm & an eventual rupture 2) Tertiary syphilis causes endarteritis of the vasa vasorum causing atrophy & giving the aorta a "Tree Bark" appearance because of the media atrophy this causes aortic root dilation resulting in aortic insufficiency (diastolic murmur) Complications: - Aortic root dilation with aortic insufficiency - Mediastinal widening - Aortic Dissection - Thoracic aneurysm

Question 39

Patho: 1) Atherosclerosis causes HTN which results atrophy of the media causing a ballooning aneurysm & an eventual rupture 2) Tertiary syphilis causes endarteritis of the vasa vasorum causing atrophy & giving the aorta a "Tree Bark" appearance because of the media atrophy this causes aortic root dilation resulting in aortic insufficiency (diastolic murmur) Complications: - Aortic root dilation with aortic insufficiency - Mediastinal widening - Aortic Dissection - Thoracic aneurysm Describes which condition?

Answer 39

Thoracic Aortic aneurysm

Question 40

Tertiary Syphilis causes what?

Answer 40

2) Tertiary syphilis causes endarteritis of the vasa vasorum causing atrophy & giving the aorta a "Tree Bark" appearance because of the media atrophy this causes aortic root dilation resulting in aortic insufficiency (diastolic murmur)

Question 41

Describe the following for Abdominal Aortic Aneurysm: What is the pathophysiology? What are the symptoms? What are the complications? What are the risk factors?

Answer 41

Patho: Atherosclerosis leads to HTN & weakness in the vessel wall. The aorta develops a balloon-like dilation that eventually ruptures (anything above 5cm!!!) Symptoms: 1) Pulsatile abdominal mass 2) Hypotension 3) Flank pain Complications: - Compression of nearby structures (i.e ureters) Risk factors: Smoking (most important risk factor) Advanced age Atherosclerosis Hypercholesterolemia and arterial hypertension

Question 42

Patho: Atherosclerosis leads to HTN & weakness in the vessel wall. The aorta develops a balloon-like dilation that eventually ruptures (anything above 5cm!!!) Symptoms: 1) Pulsatile abdominal mass 2) Hypotension 3) Flank pain Complications: - Compression of nearby structures (i.e ureters) Risk factors: Smoking (most important risk factor) Advanced age Atherosclerosis Hypercholesterolemia and arterial hypertension Describes which condition?

Answer 42

Abdominal aortic aneurysm

Question 43

Describe the following for renal stenosis: What is the pathophysiology? What are the symptoms? What are the main causes?

Answer 43

Patho: When blood flow to the kidneys is reduced causing activation of the RAAS to increase BP. One kidney is usually affected? Symptoms: 1) HTN 2) Elevated renin 3) Elevated aldosterone Causes: Atherosclerosis (older) Fibromyalgia (younger)

Question 44

Patho: When blood flow to the kidneys is reduced causing activation of the RAAS to increase BP. One kidney is usually affected. Symptoms: 1) HTN 2) Elevated renin 3) Elevated aldosterone Causes: Atherosclerosis (older) Fibromyalgia (younger) Describes which condition?

Answer 44

Renal artery stenosis

Question 45

Describe the following for Superior vena cava syndrome: What is the pathophysiology? What are the symptoms? What are the main causes of SVC?

Answer 45

Patho: Reduced blood flow to the kidneys causes it to activate the RAAS to increase BP Symptoms: 1) HTN 2) Elevated Renin 3) Elevated Aldosterone Causes: 1) Atherosclerosis (Older) 2) Fibromyalgia (Young)

Question 46

Patho: Reduced blood flow to the kidneys causes it to activate the RAAS to increase BP Symptoms: 1) HTN 2) Elevated Renin 3) Elevated Aldosterone Causes: 1) Atherosclerosis (Older) 2) Fibromyalgia (Young) Describes which condition?

Answer 46

Superior Vena cava syndrome

Question 47

Describe the following for hemangioma: What it is & where it presents?

Answer 47

A benign tumor made up of blood vessels that has cavernous vascular spaces. They usually appear on the face or liver

Question 48

A benign tumor made up of blood vessels that has cavernous vascular spaces. They usually appear on the face or liver Describes which type of tumor?

Answer 48

hemangioma

Question 49

Describe the following for Angiosarcomas: What is it? & Where does it appear? What are the key lab findings? What are the exposure risks?

Answer 49

An aggressive/metastatic tumor that is made up of endothelial cells that appear in the liver. Labs: Endothelial cells with +ve PECAM (CD31) Risks: - PVC - Arsenic - Thorium dioxide

Question 50

An aggressive/metastatic tumor that is made up of endothelial cells that appear in the liver. Labs: Endothelial cells with +ve PECAM (CD31) Risks: - PVC - Arsenic - Thorium dioxide Describes which condition?

Answer 50

Angiosarcoma

Question 51

Describe the following for Kaposi sarcoma: What is it? What are the symptoms? Who are the people at risk? What are the key lad findings?

Answer 51

A tumor that is made up of endothelial cells Symptoms: 1) Non-pruritic nodules (skin & organs) Risks: Immunocompromised - AIDS/HIV - HHV-8 - Transplant patients - European males Labs: Spindle-shaped cells Leukocyte infiltration Angiogenesis

Question 52

A tumor that is made up of endothelial cells Symptoms: 1) Non-pruritic nodules (skin & organs) Risks: Immunocompromised - AIDS/HIV - HHV-8 - Transplant patients - European males Labs: Spindle-shaped cells Leukocyte infiltration Angiogenesis Describes which condition?

Answer 52

Kaposi sarcoma

Question 53

Describe the following for Glomus tumors: What is it & where is it? What are the lab findings?

Answer 53

A benign but very painful tumor made out of smooth muscle cells underneath the nail bed or on the dorsal surface of the hand (normally involved in temperature regulation & AV shunting) Labs: Nests of round smooth muscle cells with CT Branching vascular spaces

Question 54

A benign but very painful tumor made out of smooth muscle cells underneath the nail bed or on the dorsal surface of the hand (normally involved in temperature regulation & AV shunting) Labs: Nests of round smooth muscle cells with CT Branching vascular spaces Describes which condition?

Answer 54

Glomus tumor

Question 55

Describe the following for a stable angina: What is the pathophysiology? What are the symptoms? What is the treatment?

Answer 55

Patho: Chest pain that is triggered by emotional or physical stress that lasts less than 20 minutes at a time. It is caused by atherosclerosis leading to stenosis of the coronary artery Symptoms: 1) Chest pain <20 min radiating to L.arm or jaw 2) Diaphoresis 3) SOB 4) Depressed ST segments Rx: Nitroglycerin (increases vasodilation to reduce preload)

Question 56

Patho: Chest pain that is triggered by emotional or physical stress that lasts less than 20 minutes at a time. It is caused by atherosclerosis leading to stenosis of the coronary artery Symptoms: 1) Chest pain <20 min radiating to L.arm or jaw 2) Diaphoresis 3) SOB 4) Depressed ST segments Rx: Nitroglycerin (increases vasodilation to reduce preload) Describes which condition?

Question 57

Describe the following for Unstable angina: What is the pathophysiology? What are the symptoms? What is the treatment?

Answer 57

Patho: Chest pain at rest (not triggered by exercise/stress) that lasts less than 20 minutes. Caused by atherosclerosis with thrombosis results in partial occlusion of the coronary artery. Symptoms: 1) Chest pain <20mins radiating to the L.arm & jaw 2) Diaphoresis 3) SOB 4) Occurs at rest!! Rx: Nitroglycerin (vasodilate to reduce preload of the ischemic site)

Question 58

Patho: Chest pain at rest (not triggered by exercise/stress) that lasts less than 20 minutes. Caused by atherosclerosis with thrombosis results in partial occlusion of the coronary artery. Symptoms: 1) Chest pain <20mins radiating to the L.arm & jaw 2) Diaphoresis 3) SOB 4) Occurs at rest!! Rx: Nitroglycerin (vasodilate to reduce preload of the ischemic site) Describes which condition?

Answer 58

Unstable angina

Question 59

Describe the following for prinzmetal angina: What is the pathophysiology? What are the symptoms? What is the treatment?

Answer 59

Patho: Episodic chest pain lasting no more than 20 minutes that occurs when platelets release too much thromboxane causing the coronary arteries to vasospasm Symptoms: 1) ST elevation 2) Episodic chest pain <20 minutes that radiates to the L.arm or jaw Rx: Nitroglycerin (vasodilate & reduce preload) & Ca2+ Channel blockers (reduce contractility of the heart)

Question 60

Patho: Episodic chest pain lasting no more than 20 minutes that occurs when platelets release too much thromboxane causing the coronary arteries to vasospasm Symptoms: 1) ST elevation 2) Episodic chest pain <20 minutes that radiates to the L.arm or jaw Rx: Nitroglycerin (vasodilate & reduce preload) & Ca2+ Channel blockers (reduce contractility of the heart) Describes which condition?

Answer 60

Prinzmetal angina

Question 61

Describe the following for an MI: What is the pathophysiology? - Most common cause & other causes What are the symptoms? What are the main arteries affected & what areas of the heart do they supply? What are the treatments for an MI? What are the key lab findings in an MI?

Answer 61

Patho: Onset of severe crushing chest pain lasting longer than 20 minutes leads to irreversible necrosis of myocytes. Usually caused by rupture of an atherosclerotic plaque that completely occludes the coronary artery. Other causes: - Cocaine abuse - ,Cardiomyopathies - Vasospasms Symptoms: 1) Severe/crushing Chest pain lasting longer than 20 minutes 2) Diaphoresis 3) Dyspnea Arteries: #1 LAD (supplies the ant L.vent wall & ant IVS) #2 RCA (supplies the post L.vent wall & post IVS) #3 Circumflex (supplies the lateral L.vent wall) Rx: Aspirin/Heparin (reduce thrombosis) Nitrates (vasodilation to reduce preload) ACE inhibitors (reduce LV dilation) B-blockers (Reduce contractility) Supplemental O2 (reduce ischemia) Fibrinolysis (Ca2+ influx & contractile band necrosis) Angioplasty (free radical formation & reperfusion injury) Labs: - Troponin I rises = 2-4hrs peaks = 24hrs lasts7-10 days - CK-MB rises = 4-6hrs peaks = 24hrs lasts = 72hrs

Question 62

Patho: Onset of severe crushing chest pain lasting longer than 20 minutes leads to irreversible necrosis of myocytes. Usually caused by rupture of an atherosclerotic plaque that completely occludes the coronary artery. Other causes: - Cocaine abuse - ,Cardiomyopathies - Vasospasms Symptoms: 1) Severe/crushing Chest pain lasting longer than 20 minutes 2) Diaphoresis 3) Dyspnea Arteries: #1 LAD (supplies the ant L.vent wall & ant IVS) #2 RCA (supplies the post L.vent wall & post IVS) #3 Circumflex (supplies the lateral L.vent wall) Rx: Aspirin/Heparin (reduce thrombosis) Nitrates (vasodilation to reduce preload) ACE inhibitors (reduce LV dilation) B-blockers (Reduce contractility) Supplemental O2 (reduce ischemia) Fibrinolysis (Ca2+ influx & contractile band necrosis) Angioplasty (free radical formation & reperfusion injury) Labs: - Troponin I rises = 2-4hrs peaks = 24hrs lasts7-10 days - CK-MB rises = 4-6hrs peaks = 24hrs lasts = 72hrs Describes which condition?

Answer 62

MI

Question 63

Describe the following for the MI timeline: 0-4- hrs 4-24 hrs 1-3 days 4-7 days 1-3 wks

Answer 63

0-4hrs: No gross or microscopic changes Elevated troponin I Comp: Cardiogenic shock, CHF, Arrythmia 4-24hrs: Dark discoloration Coagulative necrosis Comp: Arrythmia 1-3 days: Yellow (WBC) Neutrophil infiltration Comp: Fibrinous pericarditis (chest pain with friction rub) 4-7 days: Yellow (WBC) Macrophages infiltration Comp: Ruptures (free wall = Cardiac tamponade) (IVS = shunt) (Papillary muscles = MVP) 1-3 wks: Red border of granulation tissue (collagen, fibroblasts, & BV) Months: White scarring with fibrosis Comps: Aneurysm, Mural thrombus, & Dresslers

Question 64

Describe the following for ASD: What is the pathophysiology? - Two subtypes What are the symptoms? What are the complications?

Answer 64

Patho: A defect in the atrial septum that results in left-to-right shunting of blood & an S2 split because there's more blood in the right atria which delays the pulmonary artery from closing 1) Ostium primum is associated with Down syndrome 2) Ostium secundum is most common Symptoms: 1) S2 split 2) Pulmonary HTN Comps: Pulmonary HTN Paradoxical emboli

Question 65

Patho: A defect in the atrial septum that results in left-to-right shunting of blood & an S2 split because there's more blood in the right atria which delays the pulmonary artery from closing 1) Ostium primum is associated with Down syndrome 2) Ostium secundum is most common Symptoms: 1) S2 split 2) Pulmonary HTN Comps: Pulmonary HTN Paradoxical emboli Describes which condition?

Answer 65

ASD

Question 66

Months post MI what would you expect to find?

Answer 66

Months: White scarring with fibrosis Comps: Aneurysm, Mural thrombus, & Dresslers

Question 67

Weeks post an MI

Answer 67

1-3 wks: Red border of granulation tissue (collagen, fibroblasts, & BV)

Question 68

4-24hrs post an MI

Answer 68

4-24hrs: Dark discoloration Causative necrosis Comp: Arrythmia

Question 69

Describe the following for PDA: What is the pathophysiology? What is the associated condition? What are the symptoms? What is a complication? What is the treatment?

Answer 69

Patho: The arteriosus failed to close resulting in a left-to-right shunt between the aorta & pulmonary artery. Associated with Congenital rubella Symptoms: 1) Machine murmur Comp: Eisenmenger syndrome Rx: Indomethacin (reduce PGE to reduce the potence of PDA)

Question 70

Patho: The arteriosus failed to close resulting in a left-to-right shunt between the aorta & pulmonary artery. Associated with Congenital rubella Symptoms: 1) Machine murmur Comp: Eisenmenger syndrome Rx: Indomethacin (reduce PGE to reduce the potence of PDA) Describes which condition?

Answer 70

Patent Ductus arteriosus

Question 71

Describe the following for cardiac death syndrome: What is the pathophysiology? What is the main cause? What are the other causes?

Answer 71

Patho: Sudden death without symptoms or within 1hr of symptom onset MC: Ventricular arrythmia OC: MVP, Cocaine, & Cardiomyopathy

Question 72

Patho: Sudden death without symptoms or within 1hr of symptom onset MC: Ventricular arrythmia OC: MVP, Cocaine, & Cardiomyopathy Describes which condition?

Answer 72

Sudden cardiac death syndrome

Question 73

Describe the following for CHF for Lift sided congestive heart failure: What is the pathophysiology? What are the Symptoms? What are the labs? What are the causes? What is the treatment?

Answer 73

Patho: Decreased forward perfusion (aka systolic dysfunction) causes pulmonary congestion (blood backs up into lungs) Symptoms: 1) Pulmonary edema 2) Dyspnea 3) Hemoptysis 4) Paroxsysmal nocturnal dyspnea 5) Crackling lungs 6) HTN (activated RAAS due to low BF to kidneys) Labs: Hemosiderin-laden macrophages Causes: Ischemic HD HTN Dilated cardiomyopathy MI Restrictive cardiomyopathy Rx: ACE inhibitors (reduce LV dilation)

Question 74

Patho: Decreased forward perfusion (aka systolic dysfunction) causes pulmonary congestion (blood backs up into lungs) Symptoms: 1) Pulmonary edema 2) Dyspnea 3) Hemoptysis 4) Paroxsysmal nocturnal dyspnea 5) Crackling lungs 6) HTN (activated RAAS due to low BF to kidneys) Labs: Hemosiderin-laden macrophages Causes: Ischemic HD HTN Dilated cardiomyopathy MI Restrictive cardiomyopathy Rx: ACE inhibitors (reduce LV dilation) Describes which condition?

Answer 74

Left sided congestive heart failure

Question 75

Describe the following for right sided congestive heart failure: What is the pathophysiology? What are the symptoms? What are the causes?

Answer 75

Patho: Increased forward perfusion & hydrostatic pressure causing systemic congestion Symptoms: 1) JVD 2) Painful hepatosplenomegaly (Nutmeg liver) 3) Pitting edema Causes: #1 Left sided heart failure Left-to-right shunting Chronic lung disease (cor pumonale)

Question 76

Patho: Increased forward perfusion & hydrostatic pressure causing systemic congestion Symptoms: 1) JVD 2) Painful hepatosplenomegaly (Nutmeg liver) 3) Pitting edema Causes: #1 Left sided heart failure Left-to-right shunting Chronic lung disease (cor pumonale) Describes which condition?

Answer 76

Right sided heart failure

Question 77

Describe the following for VSD: What it the pathophysiology? What are the complications? What is the treatment?

Answer 77

Patho: The most common congenital heart defect. It's a defect in the IVS that is associated with fetal alcohol syndrome. It results in right-to-left shunting between the ventricles Comps: Eisenmenger syndrome (for large defects) Rx: Surgery or spontaneous closure

Question 78

Patho: The most common congenital heart defect. It's a defect in the IVS that is associated with fetal alcohol syndrome. It results in right-to-left shunting between the ventricles Comps: Eisenmenger syndrome (for large defects) Rx: Surgery or spontaneous closure Describes which condition?

Answer 78

VSD

Question 79

Describe the following for Tetralogy of Fallot: What is the pathophysiology? What are the symptoms? What does squatting do during cyanotic spells?

Answer 79

Patho: A combination of many structural defects (VSD, right ventricular stenosis & hypertrophy, & an aorta that overcomes VSD) it results in a right-to-left shunt & early cyanosis Symptoms: 1) Early cyanosis 2) Boot shaped heart 3) Cyanotic spells Rx: Squatting increases peripheral arterial resistance to decrease shunting to keep more blood oxygenated during a cyanotic spell

Question 80

Patho: A combination of many structural defects (VSD, right ventricular stenosis & hypertrophy, & an aorta that overcomes VSD) it results in a right-to-left shunt & early cyanosis Symptoms: 1) Early cyanosis 2) Boot shaped heart 3) Cyanotic spells Rx: Squatting increases peripheral arterial resistance to decrease shunting to keep more blood oxygenated during a cyanotic spell Describes which condition?

Answer 80

Tetralogy of Fallot

Question 81

Describe the following for Truncus arteriosus: What is the pathophysiology? What is a symptom

Answer 81

Patho: The truncus didn't divide so that the aorta & pulmonary artery arise from one blood vessel from both ventricles so O2 rich & poor blood mixes before being sent into circulation Symptoms: 1) Early cyanosis

Question 82

Patho: The truncus didn't divide so that the aorta & pulmonary artery arise from one blood vessel from both ventricles so O2 rich & poor blood mixes before being sent into circulation Symptoms: 1) Early cyanosis Describe which condition?

Answer 82

Truncus arteriosus

Question 83

Describe the following for Tricuspid Atresia: What is the pathophysiology? What is the symptom?

Answer 83

Patho: The tricuspid valve orifice doesn't develop resulting in a hypoplastic right ventricle causing a left-to-right shunt that is associated with an ASD Symptom: 1) Early cyanosis

Question 84

Describe the following for coarctation of the aorta: What is the pathophysiology? - subtypes What are the symptoms? -subtypes

Answer 84

Patho: A narrowed/pinched segment of the aorta that has two forms 1) Infantile form that sits after the aortic arch & before the PDA (associated with PDA & Turners) 2) Adult form that sits after the aortic arch (associated with a bicuspid aortic valve) Symptoms: Infantile 1) Cyanosis in the lower extremities Adult 1) HTN in the upper extremity 2) Hypotension & weak pulse in the lower extremities 3) Collateral circulation in the intercostal arteries 4) Engorged arteries

Question 85

Patho: A narrowed/pinched segment of the aorta that has two forms 1) Infantile form that sits after the aortic arch & before the PDA (associated with PDA & Turners) 2) Adult form that sits after the aortic arch (associated with a bicuspid aortic valve) Symptoms: Infantile 1) Cyanosis in the lower extremities Adult 1) HTN in the upper extremity 2) Hypotension & weak pulse in the lower extremities 3) Collateral circulation in the intercostal arteries 4) Engorged arteries

Answer 85

coarctation of the aorta

Question 86

Describe the following for acute rheumatic fever: What is the pathophysiology? - MOA of the pathogen What are the symptoms - Major jones criteria - Minor jones criteria What is the major cause of death? What is a complication?

Answer 86

Patho: A systematic complication of pharyngitis due to group A B-hemolytic streptococcus that usually happens in 2-3yr olds MOA of group A B hemolytic strep: Uses molecular mimicry via their M protein to cause a type III hypersensitivity reaction Symptoms: Major Jones 1) Elevated AS/Anti-DNase titre 2) Migratory polyarthritis 3) Pancarditis - Endocarditis (mitral valve regurg/insufficiency) - Myocarditis (Aschoff bodies) - Pericarditis (friction rub + chest pain) 4) Subcutaneous nodes 5) Erythema marginatum 6) Sydenham chorea (involuntary move) Minor: 1) Fever 2) Elevated ESR COD: Myocarditis Comp: Progresses to chronic rheumatic heart disease with repeated exposure

Question 87

Patho: A systematic complication of pharyngitis due to group A B-hemolytic streptococcus that usually happens in 2-3yr olds MOA of group A B hemolytic strep: Uses molecular mimicry via their M protein to cause a type III hypersensitivity reaction Symptoms: Major Jones 1) Elevated AS/Anti-DNase titre 2) Migratory polyarthritis 3) Pancarditis - Endocarditis (mitral valve regurg/insufficiency) - Myocarditis (Aschoff bodies) - Pericarditis (friction rub + chest pain) 4) Subcutaneous nodes 5) Erythema marginatum 6) Sydenham chorea (involuntary move) Minor: 1) Fever 2) Elevated ESR COD: Myocarditis Comp: Progresses to chronic rheumatic heart disease with repeated exposure Describes which condition?

Answer 87

Acute Rheumatic heart disease

Question 88

Describe the following for chronic rheumatic heart disease: What is the pathophysiology? What are the symptoms? What is a concerning sequelae?

Answer 88

Patho: Chronic inflammation in response to group A B-hemolytic strep (repeated exposures) results in scarring of the heart valves & thickening of chordae tendinea causing Mitral valve stenosis (less commonly affects the aortic) Symptoms: 1) Mitral stenosis 2) Aortic stenosis (less common) 3) Fish mouth valve Sequelae: Infectious endocarditis (usually with S. viridians

Question 89

Patho: Chronic inflammation in response to group A B-hemolytic strep (repeated exposures) results in scarring of the heart valves & thickening of chordae tendinea causing Mitral valve stenosis (less commonly affects the aortic) Symptoms: 1) Mitral stenosis 2) Aortic stenosis (less common) 3) Fish mouth valve Sequelae: Infectious endocarditis (usually with S. viridians Describes which condition?

Answer 89

chronic rheumatic heart disease

Question 90

Describe the following for aortic stenosis: What is the pathophysiology? What are the cardiac changes that occur? What are the symptoms? What are the causes? - most common - less common

Answer 90

Patho: The aortic valve becomes narrowed/stidd due to fibrosis & calcification for the most part. This results in a reduced ejection fraction from the left ventricle & cardiac changes Cardiac changes: Left ventricular hypertrophy (to try to increase the ejection fraction) Symptoms: 1) Syncope with exercise (L.vent hypertrophy & low EF%) 2) Left ventricular hypertrophy 3) Microangiopathic hemolytic anemia 4) Systolic ejection click followed by a crescendo-decrescendo murmur Causes: MC (Fibrosis & calcification (stenosis) & bicuspid aortic valve (wear/tear) LC (CRHD (scarring))

Question 91

Patho: The aortic valve becomes narrowed/stidd due to fibrosis & calcification for the most part. This results in a reduced ejection fraction from the left ventricle & cardiac changes Cardiac changes: Left ventricular hypertrophy (to try to increase the ejection fraction) Symptoms: 1) Syncope with exercise (L.vent hypertrophy & low EF%) 2) Left ventricular hypertrophy 3) Microangiopathic hemolytic anemia 4) Systolic ejection click followed by a crescendo-decrescendo murmur Causes: MC (Fibrosis & calcification (stenosis) & bicuspid aortic valve (wear/tear) LC (CRHD (scarring)) Describes which condition?

Answer 91

Aortic Stenosis

Question 92

Describe the following for Aortic regurgitation/insufficiency: What is the pathophysiology? What are the symptoms? What are the causes? What are the treatments?

Answer 92

Patho: The aortic valves can't close completely causing blood to leak back into the left ventricle during diastole resulting in left ventricular dilation & hypertrophy due to the fluid overload. Symptoms: 1) An early blowing diastolic murmur 2) Hyperdynamic circulation 3) Bounding "water hammer" pulse 4) Quincke pulse (nail bed) 5) Head bobbing Cause: #1 Aortic root dilation (due to syphilis or aortic dissection)

Question 93

Patho: The aortic valves can't close completely causing blood to leak back into the left ventricle during diastole resulting in left ventricular dilation & hypertrophy due to the fluid overload. Symptoms: 1) An early blowing diastolic murmur 2) Hyperdynamic circulation 3) Bounding "water hammer" pulse 4) Quincke pulse (nail bed) 5) Head bobbing Cause: #1 Aortic root dilation (due to syphilis or aortic dissection) Describes which condition?

Answer 93

Aortic regurgitation/insufficiency

Question 94

Describe the following for mitral valve prolapse: What is the pathophysiology? What are the symptoms? What is the treatment? -what effect does squatting cause What are the associated conditions?

Answer 94

Patho: There is ballooning of the mitral valve into the left atrium during systole, resulting in a mid-systolic click followed by a regurgitation murmur. Myxoid degeneration causes an accumulation of the ground substance on the valves make it floppy. Symptoms: 1) Mid-systolic click followed by a regurgitation murmur Rx: Valve replacement Squatting makes the mid-systolic click softer because of an increase in peripheral vascular resistance to decrease the left ventricular filling Comps: Marfan's & Ehler-Danlos syndrome (CT disorders)

Question 95

Patho: There is ballooning of the mitral valve into the left atrium during systole, resulting in a mid-systolic click followed by a regurgitation murmur. Myxoid degeneration causes an accumulation of the ground substance on the valves make it floppy. Symptoms: 1) Mid-systolic click followed by a regurgitation murmur Rx: Valve replacement Squatting makes the mid-systolic click softer because of an increase in peripheral vascular resistance to decrease the left ventricular filling Comps: Marfan's & Ehler-Danlos syndrome (CT disorders) Describes which condition?

Answer 95

mitral valve prolapse

Question 96

Describe the following for Mitral regurgitation/insufficiency: What is the pathophysiology? What are the symptoms? - squatting has what effect? What are the causes? - main cause - other

Answer 96

Patho: When the mitral valve can't close fully so that blood leaks back into the left atrium during systole resulting in fluid overload & dilation Symptoms: 1) Holosystolic blowing murmur (louder when squatting) Squatting causes the murmur to be louder because the increase in systemic resistance decreases left ventricular emptying Causes: MC = MVP Other = Infective endocarditis (s. viridans) Acute rheumatic heart disease Papillary muscle rupture post MI Non-infective endocarditis (Libman sacs)

Question 97

Patho: When the mitral valve can't close fully so that blood leaks back into the left atrium during systole resulting in fluid overload & dilation Symptoms: 1) Holosystolic blowing murmur (louder when squatting) Squatting causes the murmur to be louder because the increase in systemic resistance decreases left ventricular emptying Causes: MC = MVP Other = Infective endocarditis (s. viridans) Acute rheumatic heart disease Papillary muscle rupture post MI Non-infective endocarditis (Libman sacs) Describes which condition?

Answer 97

Mitral valve regurgitation/insufficiency

Question 98

Describe the following for mitral valve stenosis: What is the pathophysiology? What are the symptoms? What are the causes? What is a complication? - sequelae

Answer 98

Patho: A narrowed mitral valve results in an open snap & diastolic rumble due to fluid overload dilating the left atrium causing pulmonary congestion Symptoms: 1) Open snap & diastolic rumble 2) Dilated left atrium 3) Pulmonary edema 4) Hemoptysis 5) Pulmonary HTN & right sided HF 6) A fibrillation Causes: Chronic rheumatic heart disease Sequelae: A fibrillation can progress to a mural thrombosis

Question 99

Patho: A narrowed mitral valve results in an open snap & diastolic rumble due to fluid overload dilating the left atrium causing pulmonary congestion Symptoms: 1) Open snap & diastolic rumble 2) Dilated left atrium 3) Pulmonary edema 4) Hemoptysis 5) Pulmonary HTN & right sided HF 6) A fibrillation Causes: Chronic rheumatic heart disease Sequelae: A fibrillation can progress to a mural thrombosis Describes which condition?

Answer 99

mitral valve stenosis

Question 100

Describe the following for Bacterial endocarditis due to S. viridians: What is the pathophysiology? What is a symptom? What are the associated conditions? What is the treatment?

Answer 100

Patho: Because it has low virulence it can only infect heart valves that have already been damaged especially the MITRAL valve. It grows vegetations (fibrin & platelets) on the valves to trap bacteria and cause inflammation Symptom: 1) Mitral insufficiency (holosystolic murmur) 2) Splinter hemorrhages (nails) 3) Osler nodes (ouch) 4) Janeway lesions 5) Roth spots Ass conditions: Chronic rheumatic heart disease MVP

Question 101

Patho: Most common Because it has low virulence it can only infect heart valves that have already been damaged especially the MITRAL valve. It grows vegetations (fibrin & platelets) on the valves to trap bacteria and cause inflammation Symptom: 1) Mitral insufficiency (holosystolic murmur) 2) Splinter hemorrhages (nails) 3) Osler nodes (ouch) 4) Janeway lesions 5) Roth spots Ass conditions: Chronic rheumatic heart disease MVP

Answer 101

Bacterial endocarditis infected with S viridians

Question 102

Describe the following for bacterial endocarditis infected with S. aureus: What is the pathophysiology? What are the symptoms?

Answer 102

Patho: Most common among IV drug abusers. It is very virulent so it can infect healthy heart valves (TRICUSPID). It grows vegetations which destroy the valve Symptoms: Symptom: 1) Tricuspid insufficiency (holosystolic murmur) 2) Splinter hemorrhages (nails) 3) Osler nodes (ouch) 4) Janeway lesions 5) Roth spots

Question 103

Patho: Most common among IV drug abusers. It is very virulent so it can infect healthy heart valves (TRICUSPID). It grows vegetations which destroy the valve Symptoms: Symptom: 1) Tricuspid insufficiency (holosystolic murmur) 2) Splinter hemorrhages (nails) 3) Osler nodes (ouch) 4) Janeway lesions 5) Roth spots Describes which condition?

Answer 103

Bacterial endocarditis with S. aureus