All Block 1 materials (overview from cardiovascular-pulmonary) Flashcards
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?
Nasal polyps
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?
Allergic rhinitis
Describe what Rhinitis is, how it presents, & what the most common cause of it is
When the nasal mucosa becomes inflamed, usually due to the rhinovirus
Signs: Sneezing, Congestion, Runny nose/coughing
Explain what allergic rhinitis is? What conditions is it associated with?
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
Describe what a nasal polyp is?
What causes it?
What conditions is it associated with?
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
Describe the following for Takayasu’s disease:
What is the pathophysiology?
What are the symptoms?
What artery is most likely affected?
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
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?
Takayasu’s disease
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?
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
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?
Wegener’s granulomatosis
Describe the following for microscopic polyangiitis:
What is the pathophysiology?
What are the symptoms?
What is a key lab finding?
What is the treatment?
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
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?
microscopic polyangiitis
Describe the following for Cryoglobulinemia:
What is the pathophysiology?
What are the symptoms?
What are the lab findings?
Patho:
Vasculitis triggered by a prior Hep C infection
Symptoms:
1) Hematuria
2) Palpable purpura
3) Arthralgia
Labs:
Hep C & Cryoglobulin deposits
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?
Cyroglobulinemia
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?
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
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?
Kawasaki disease
Describe the following for Churg-Strauss syndrome:
What is the pathophysiology?
What are the symptoms?
What are the lab findings?
What is the treatment?
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
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?
Churg-Strauss Syndrome
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?
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
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?
Polyarteritis Nodosa
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?
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
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?
Giant cell (temporal) arteritis
Describe the following for Henoch-Schönlein Purpura:
What is the pathophysiology?
What are the symptoms?
What are the lab findings?
What is the treatment?
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)
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?
Henoch-Schönlein Purpura
Describe the following for thromboangitis obliterans:
What is the pathophysiology?
What are the symptoms?
-early
-late
What is the treatment?
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
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?
Thromboangitis obliterans
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
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
Describe the following for arteriosclerosis:
What is the pathophysiology?
What are the two subtypes?
What are the complications of the subtypes?
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)
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?
Arteriosclerosis
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?
Hyaline Arteriosclerosis
Describe the pathophysiology of Hyaline arteriosclerosis
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)
Caused by malignant hypertension resulting in smooth muscle cell proliferation giving it an onion skin appearance
Describes which condition?
Hyperplastic arteriosclerosis
Describe the pathophysiology of hyperplastic arteriosclerosis
Caused by malignant hypertension resulting in smooth muscle cell proliferation giving it an onion skin appearance
What are the main arteries impacted by atherosclerosis?
** Abdominal aorta
Coronary arteries
Popliteal arteries
Descending thoracic aorta
Internal carotid artery
Describe what Monkenberg-medial-calcification is?
It’s non-obstructive calcification of the media that is NOT clinically significant
It’s non-obstructive calcification of the media that is NOT clinically significant
Monkenberg-medial-calcification
Describe the following for Aortic Dissection:
What is the pathophysiology?
- Two major causes
What are the symptoms?
What are the complications?
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)
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?
Aortic dissection
Describe the following for a Thoracic aneurysm:
What is the pathophysiology?
- Two major causes
What are the symptoms?
What are the complications?
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
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?
Thoracic Aortic aneurysm
Tertiary Syphilis causes what?
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)
Describe the following for Abdominal Aortic Aneurysm:
What is the pathophysiology?
What are the symptoms?
What are the complications?
What are the risk factors?
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
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?
Abdominal aortic aneurysm
Describe the following for renal stenosis:
What is the pathophysiology?
What are the symptoms?
What are the main causes?
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)
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?
Renal artery stenosis
Describe the following for Superior vena cava syndrome:
What is the pathophysiology?
What are the symptoms?
What are the main causes of SVC?
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)
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?
Superior Vena cava syndrome
Describe the following for hemangioma:
What it is & where it presents?
A benign tumor made up of blood vessels that has cavernous vascular spaces. They usually appear on the face or liver
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?
hemangioma
Describe the following for Angiosarcomas:
What is it? & Where does it appear?
What are the key lab findings?
What are the exposure risks?
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
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?
Angiosarcoma
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?
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
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?
Kaposi sarcoma
Describe the following for Glomus tumors:
What is it & where is it?
What are the lab findings?
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
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?
Glomus tumor
Describe the following for a stable angina:
What is the pathophysiology?
What are the symptoms?
What is the treatment?
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)
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?
Describe the following for Unstable angina:
What is the pathophysiology?
What are the symptoms?
What is the treatment?
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)
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?
Unstable angina
Describe the following for prinzmetal angina:
What is the pathophysiology?
What are the symptoms?
What is the treatment?
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)
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?
Prinzmetal angina
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?
2 RCA (supplies the post L.vent wall & post IVS)
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)
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
2 RCA (supplies the post L.vent wall & post IVS)
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)
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?
MI
Describe the following for the MI timeline:
0-4- hrs
4-24 hrs
1-3 days
4-7 days
1-3 wks
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
Describe the following for ASD:
What is the pathophysiology?
- Two subtypes
What are the symptoms?
What are the complications?
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
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?
ASD
Months post MI what would you expect to find?
Months:
White scarring with fibrosis
Comps: Aneurysm, Mural thrombus, & Dresslers
Weeks post an MI
1-3 wks:
Red border of granulation tissue (collagen, fibroblasts, & BV)
4-24hrs post an MI
4-24hrs:
Dark discoloration
Causative necrosis
Comp: Arrythmia
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?
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)
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?
Patent Ductus arteriosus
Describe the following for cardiac death syndrome:
What is the pathophysiology?
What is the main cause?
What are the other causes?
Patho:
Sudden death without symptoms or within 1hr of symptom onset
MC: Ventricular arrythmia
OC: MVP, Cocaine, & Cardiomyopathy
Patho:
Sudden death without symptoms or within 1hr of symptom onset
MC: Ventricular arrythmia
OC: MVP, Cocaine, & Cardiomyopathy
Describes which condition?
Sudden cardiac death syndrome
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?
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)
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?
Left sided congestive heart failure
Describe the following for right sided congestive heart failure:
What is the pathophysiology?
What are the symptoms?
What are the causes?
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)
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?
Right sided heart failure
Describe the following for VSD:
What it the pathophysiology?
What are the complications?
What is the treatment?
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
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?
VSD
Describe the following for Tetralogy of Fallot:
What is the pathophysiology?
What are the symptoms?
What does squatting do during cyanotic spells?
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
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?
Tetralogy of Fallot
Describe the following for Truncus arteriosus:
What is the pathophysiology?
What is a symptom
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
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?
Truncus arteriosus
Describe the following for Tricuspid Atresia:
What is the pathophysiology?
What is the symptom?
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
Describe the following for coarctation of the aorta:
What is the pathophysiology?
- subtypes
What are the symptoms?
-subtypes
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
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
coarctation of the aorta
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?
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
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?
Acute Rheumatic heart disease
Describe the following for chronic rheumatic heart disease:
What is the pathophysiology?
What are the symptoms?
What is a concerning sequelae?
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
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?
chronic rheumatic heart disease
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
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))
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?
Aortic Stenosis
Describe the following for Aortic regurgitation/insufficiency:
What is the pathophysiology?
What are the symptoms?
What are the causes?
What are the treatments?
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)
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?
Aortic regurgitation/insufficiency
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?
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)
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?
mitral valve prolapse
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
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)
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?
Mitral valve regurgitation/insufficiency
Describe the following for mitral valve stenosis:
What is the pathophysiology?
What are the symptoms?
What are the causes?
What is a complication?
- sequelae
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
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?
mitral valve stenosis
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?
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
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
Bacterial endocarditis infected with S viridians
Describe the following for bacterial endocarditis infected with S. aureus:
What is the pathophysiology?
What are the symptoms?
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
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?
Bacterial endocarditis with S. aureus
