Exam 2 Flashcards
Decrease in collagen synthesis Increase in collage degradation Increase in macrophages and T-cells Decrease in smooth muscle cells.
Factors that weaken the capsule
Severe and acute onset of HTN (>200/>110), patients experience severe headaches and bleed.
Malignant Hypertension
Occurs from organisms in the community rather than from the hospital
Infection starting outside the hospital or within 48 hours of admission in a pt not residing in a long-term care facility for at least 14 days before admission
Bacterial or viral (what are they?)
CAP
*S. pneumoniae, H. flu, S. aureus, mycoplasma, chlamydia, or influenza
A 25 year old patient comes in with headache (migraine), fever, malaise, hypertension, gangrene, and peripheral nerve damage. It appears that the symptoms are episodic and recurrent. It appears the small and medium arteries are affected and the patient is suffering from necrotizing inflammation. The kidney, skin on the legs, heart, liver and GI tract have been affected. The patient also appears to be suffering from GI bleeding, renal failure, muscle aches, skin ulcers, neuritis, and hepatitis. You ask the patient if they have ever been tested for Hep C, B and cryoglobulins which can cause this disease. The patient is suffering from hematuria because the small vessels are affected. The lungs are not affected. A biopsy shows patchy inflammation of all three layers. You are concerned this may lead to a heart attack or stroke.
Polyarteritis Nodosa (PAN)
Involves the mucus membranes, skin, and deep organs (lungs).
Pt presents with oral thrush, esophagitis, omychomycosis, renal abscess, meningitis, pneumonia/ pneumonitis, liver abscess
Candida Pneumonia
True Type Diffuse Circumferential
Fusiform Aneurysm
Anything that increases CO and/or SVR
Chronic HTN will result in IHD, CVA, CHF, Renal failure, aortic dissection, LV hypertrophy
Hypertensive Vascular Disease (HTN)
Males have a much greater risk until women hit menopause (pre-menopause one has the protective effects of estrogen)
How is gender a non-modifiable risk of atherosclerosis?
Inflammation and infection of the lung parenchymal structures or the alveoli.
There are 3 methods of classification:
setting (which consists of what?)
etiology (which is what?)
distribution (which is what?)
Pneumonia
*CAP or HAP
*typical or atypical
*lobar, bronchopneumonia or intersitial
Viral infection (cosaxie, echovirus)
Bacterial (TB, strep, staph)
Fungal
Secondary to an AMI
Due to radiation to the chest
Uremia (most common systemic disorder)
SLE
Cardiac Surgery
Causes of pericarditis
Inflammatory exudative or transudative fluid between pericardial layers.
Increased permeability with weeping fluid and proteins due to the inflammation
Effusion can develop.
2 layers are affected: visceral and parietal
Pathophysiology of pericarditis
Abnormal communication between chambers or vessels.
Pressure differential determines the flow pattern.
There is mixing between venous and arterial blood.
Connection between 2 chambers.
V/Q mismatch in the blood
Shunt
What is at high risk or rupture, erosion, and hemorrhage into the atheroma? There are a large number of foam cells and extracellular lipids. There is a thin fibrous capsule, few smooth muscles, and a cluster of inflammatory cells. There is also little amount of collagen due to what enzymes?
Vulnerable Plaque *MMPs
Decreased filling of the ventricle
Diminished compliance
40% CHF
More common in women and older patients
HTN and DM have more of this dysfunction
Higher ventricular pressure at any given volume
Tachycardia worsens this type of heart failure
Diastolic heart failure
Identifiable etiology (5-10%): renal, endocrine, vascular, and neurogenic.
It is correctable or reversible, seen in younger persons, and may present with higher BP and acute
Many factors that influence CO, SVR and Bp can be primarily disrupted by disease processes. Volume status (kidney disease and poor Na handling), Angiotension II, aldosterone, and adrenergic tone
Secondary Hypertension
Aortic stenosis
mirtal valve regurgitation
pulmonic stenosis
tricuspid regurgitation
all cause what?
Systolic murmur
Rhinotracheitis, viral pneumonia, secondary bacterial infection can cause this. The virus attaches to the MM epithelium, killing mucus secreting and muco-ciliary lining, which creates gaps between protective epithelium, allowing ECF to escape (runny nose). The lining of the trachea, bronchi, and alevoli are shedded if what? The pt appears to be suffering from intersitial pneumonia with inflammation between the alveoli. This enhances the bacterial adhesion to the epithelium.
Influneza Pathophysiology
*viral pneumonia
Left ventricular hypertrophy and massive thickening of the ventricular septum.
The patient will exhibit abnormal diastolic filling causing intermittent LV outflow obstruction, arrhythmias, and sudden death in young athletes. Impaired filling results in reduced SV and CO. Obstruction is exaggerated by increased myocardial contraction (sympathetic) and decreased ventricular filling (Valsalva, venous pooling).
This is genetic autosomal dominant
Occurs in the abscence of increased afterload
Asymmetric septal hypertrophy with LV outflow obstruction.
Valsalva: decreased preload: increases systolic murmur
Diastolic dysfunction causing decrease in filling due to stiff ventricles
Hypertrophic cardiomyopathy
May rupture or erode with platelet adhesion and thrombus
Unstable angina or acute MI is the result
What are the vulnerability factors?
Triggered by sympathetic activity and platelet adhesion: rapid rise in BP or HR, stress
Occurs within the first hour of waking up
Unstable or vulnerable plaque
*large lipid core with small fibrous cap, inflammation, and lack of stabilizing smooth msucle cells (low collagen)
Advanced lesions with hemorrhage, ulceration or erosion which often results in platelet activation, thrombosis formation on top of plaque with acute occlusion of arterial flow. Type of atherosclerosis plaque
Complex plaque
Younger men more than younger women Blacks more than whites Lower socioeconomics Older persons (increases with age) Men more than women until menopause
Who hypertension affects?
120-139/80-89
Pre-hypertension
Largest single cause of Secondary HTN due to the increased salt and water retention, decreased urine formation, and HTN.
Glomerulonephritis
Acute renal failure
Diabetic nephropathy
Chronic renal failure
Renovascular HTN
RAS is activated producing high renin levels and AT2.
What are the two major types?
Renal HTN
*Atherosclerosis, fibromuscular dyplasia (women, thrid decade of life, family history, smoking, and dyslipidemia
Adrenal medulla tumor causing excessive catecholamine secretion (Epi and NE).
90% are benign
Patient will have episodic symptoms which are?
Urine catecholamine collections, CT or MRI of adrenals, and serum epi levels
Pheochromocytoma
*headache, sweating, palpitations, tremor, weight loss, swings of severe HTN, nervousness, and weakness
Typical of malignant HTN, acute/severe elevations of blood pressure.
Hyperplastic chagnes
Fibrinoid deposits
Vessel wall necrosis
Prominent n kidney and cerebral vessels
Hyperplastic atheriosclerosis
Determine cause of HF
LV systolic failure or HFPEF
Potential findings are?
Echocardiography for Heart failure
*Ventricular hypertrophy, valvular abnormalities, effusion, PAH
Caused by viruses or mycoplasma or chlamydia
Pathogens invade the alveolar septum and interstitum of lung
“Walking pneumonia”
Protracted course and less purulent sputum
Inflammation of the alveolar septa, pulmonary interstitium, and capillary-alveolar wall
Dry cough: scant sputum
Patchy infiltrates: interstitial patterns
Etiology: mycoplasma and virus (which ones?)
Atypical pneumonia
*RSV, Influenza, and Adenovirus
Often autoimmune induced (SLE)
Lack of response to NSAIDS
Use of corticosteroids increase the recurrence if used in the first aatack
Recurrent pericarditis
It forms in the intima layer which is beneath the endothelium It eventually encroaches on the lumen and reduces blood flow
Mechanism of plaque formation?
Increases CO independent of preload and afterload
Calcium diffuses into myocardial cells, which promotes sliding of actin and myosin. This opens L-type Ca channels. Catecholamines and Na/Ca exchange pump
Contractility
160 high
LDL cholesterol levels
Hypervolemia (which is caused by?)
Stress: sympathetic activation
Pheochromocytoma: increased catecholamines
What increases the cardiac output?
*renal artery stenosis, renal disease, hyperaldosteronism, hypersecretion of ADH, pregnancy, or aortic coarctation
Between 40-60 yo: 5-fold increase in AMI in men Plaques have been evolving long before clinical symptoms and significance
How is age a non-modifiable risk factor to atherosclerosis?
The less common type of thoracic aorta dissection Distal to take-off of major vessels Descending only Less complications This is above the diaphragm, manage conservatively, and it doesn’t involved the neck and head.
Type B: III
Supprative and exudative
Bacterial
Fibrinopurulent
Caused by bacteria that invades the alveoli and results in pus formation. Pus is composed of what?
Lobar or patchy consolidation of lung segments
High fever, rigors, rusty sputum, and productive exudate
Typical Pneumonia
*PMNs, bacteria, edema, RBC, and protein exudate
Close contact with known case of this
HIV infection
Birth in a country with high prevalence of this
Homelessness
Residence in long-term care facilities and correctional facilities
Intravenous drug user
Risk factors for TB
Fungus: pneumoncystis jiroveci
Immune suppression: Low CD4 counts
Causes interstitial pneumonitis, fever, bilateral infiltrates, dyspnea, hypoxia is common
Restrictive lung disease
Use sputum culture to identify pathogen
PCP
Age, male gender, smoking, family history, Ehler’s Danlos
Abdominal Aortic Aneurysm Risk Factors
Heart
Kidney
Eyes
Brain
Blood vessels
Atherosclerosis: CAD, CHF, CVA, PVD
LV hypertrophy (contrast with what?): adaptation (non-physiological), high afterload (increased workload on heart), and risk factors for what?
Organs that HTN target
*exercise
*CAD, arrhythemia, sudden death, CHF
This is the most common type of thoracic aorta dissection . There are proximal lesions which can occur in the ascending or descending or both. This is more dangerous and has a higher risk of rupture. It can get into valve.
Type A: Debakey I &II
bleeding within the vulnerable plaque substance, which results in what?
Hemorrhage *acute enlargement of plaque with subsequent obstruction and ischemia later
Immune complex deposition (SLE, Drug hypersensitivity, and infection mediated) Anti-neutrophil-cytoplasmic antibodies (ANCA) Anti-endothelial cell antibodies
The immune mechanisms of vasculitis
50% of all AMI
Infarction and necrosis occurs in the anterior wall of the left ventricle, anterior 2/3 of the ventricular septum, and the majority of the apex of the heart
LAD Occlusion
Blood volume via sodium levels and the release of aldosterone and ANP.
Cardiac Factors: contractility (inotropic) and heart rate
Modulators of CO
Interstitial inflammatory infiltrate
myocyte injury
lymphocyctic or mononuclear infiltrate is common
Patchy involvement
Not as many PMNs
Pathology findings of myocarditis
Patient comes in with chest pain after exertion. They say they experience relief with rest or a dose of nitroglycerin.
They appear to have predictable symptoms
You know that this does not require evaluation or medication because the plaque is fixed. You can watch and follow the patient
Stable angina
Progressive cardiac decompensation (CHF) following AMI
Myocardial necrosis results in heart muscle dysfunction
Chronic IHD
Syndrome 3
A patient comes in with dyspnea, chest pain, atrial fibrilation (Why does this occur?), and appears to be at risk for embolization of mural thrombosis. You examine the patient and find fibrosis replacement of valve with stiffness. There is left artial enlargement with elevated pressure, pulmonary congestion, pulmonary edema, decreased LV filling during diastole, creating a diastolic murmur (heard when?). What does the patient have?
Mitral valve stenosis
*The dilation of the ventricles cause the stretch receptors are triggered and makes the heart want to pump more.
*S1 and S2
Asymtomatic until adulthood
Initially left to right shunt
If it is not corrected then pulmonary HTN occurs due to the high pressure and volume on the right side and Eisenmenger’s develops
ASD
Most frequent cause of gram negative pneumonia
Debilitated, Nursing home pts, alcoholics
Klebsiella
Stress: sympathetic activation
Atherosclerosis
Renal artery disease: increased angiotension II
Pheochromocytoma
Thyroid dysfunction
Diabetes
Cerebral ischemia
Increase Systemic vascular resistance
High Salt intake
Excessive ETOH
Obesity/ high calorie intake: central obesity
Smoking: not an independent risk factor, related to increased CAD and HTN
Stress
Lifestyle Risks of Primary HTN
A patient comes in with fever, chest pain, fatigue,dyspnea, signs of CHF, and arrhythmia. What are the three outcomes? You explain to the patient they are experiencing an infection or inflammation of the myocardium. Virus infections are the most common cause of this in the US. What viruses cause this? The cause was either direct viral or an autoimmune response to the agent. Malignant arrhytmia and systolic heart failure are two outcomes you try to avoid.
Myocarditis
*minor symptom and resolution, progressive CHF, and lethal outcome
*Coxsackie, Enterovirus, CMV, HIV
Patient comes in with fever, bacteremia, and chills. You listen to their heart and they have a new heart murmur. The patient appears to be lethargic. The patient is also coughing, experiencing dyspnea, and arthagias. There appears to be an embolic distribution of vegetative lesions, splinter hemorrhages in the skin and nail beds. The patient also exhibits Roth spots, Osler nodes, and Janeway lesions.
Endocarditis
Pt comes in with rapid progression of fever, tachypnea, tachycardia, cyanosis with hypoxemia.
Interstitial pneumonitis
Bacterial pneumonia is a common complication, which is caused by what bugs?
Viral Pneumonia: Influenza
*S.pneumoniae, M. catarrhalis, H. flu
Localized dilation of a blood vessel, arteries (which one is the most common?) There are true and false types. It occurs usually when there is a tear in the intima allowing blood to enter the vessel wall. Blood will move between layers of the media, creating a false lumen within the media.
Aneurysm *Aorta
Increases BP and decreases myocardial O2 supply Adverse hemostatic and inflammatory effects Enhances LDL oxidation which leads to what? **Nicotine is a vasoconstrictor which will cause coronary constriction, which becomes a problem when plaques build later in life.
Smoking *endothelial damage
Essential, chronic elevation over time, no other identified etiology, and 90% of all cases.
Primary Hypertension
First symptom in RF
Affects the large joints
Ranges from mild pain to disabling arthritis
3-4 weeks and will respond to what?
Polyarthritis
*Aspirin
Smoking Hyperlipidemia Hypertension Diabetes C-reactive protein (inflammation) Obesity Sedentary lifestyle Fat and carbohydrates Stress: adrenergic response
What are the modifiable risk factors of atherosclerosis?
A patient comes in with fever, myalgia, arthralgia, and malaise. For more specific symptoms the specific vessel has to be determined. Group of vascular disorders that cause inflammatory injury and necrosis of the blood vessel wall. Any vessel can be involved. What are the three classifications? And what are the two most common mechanism?
Vasculitis *Small, medium and large vessels * inflammation and infection
25% protein 50% cholesterol 10% triglycerides 60% back to the liver/ 40% extra-hepatic tissues Bad cholesterol: essentially the primary element that takes fats, glycerol and places them as plaque in the vessel wall taken up by scavenger receptors if saturated these are located where? if cholesterol is taken up by macrophages in vessel walls what forms? rich in esters and cholesterol adrenal and gonads
LDL *endothelial cells * atheromatous formation
Gives of diagonal branches that feed the left anterior wall, anterior septum, and anterior papilary muscles
LAD
subsequent thrombosis and ischemia
Erosion of plaque
Can result from lethal arrhythmias following AMI
Usually from sustained ventricular arrhythmia
CAD 90% of cause this
Younger victims: hereditary conduction abnormalities, myocarditis or sarcoidosis, hypertrophic cardiomyopathym and pulmonary hypertension
30-40% of IHD first symptom is death
Sudden Cardiac Death Syndrome 4
cholesterol esters and triglycerides are in the center: hydrophobic shell of hydrophilic phospholipids, cholesterol, and apoproteins apoproteins are recognized by receptors (if these are affected by a genetic disorder what will occur?)
What is the structure of a lipoprotein? (Atherosclerosis)
Pericarditis
Polyarthritis
Chorea
Subcutaneous nodules
Erythema marginatum
Must have 2 of these or 1 plus a minor to be what?
Major criteria for RF
*RF
Renovascular HTN
Adrendal induced HTN
Pheochromocytoma
Coarctation of aorta
OCP induced
Cocaine/Amphetamine induced
Most common secondary causes
plaque rupture with thrombogenic emboli and will cause what?
Embolization *acute ischemia
One-time US screening for AAA for all men (what age?) who have ever smoked Elective repair for AAA at 5.5 cm or > or if >0.5 cm expansion in one year is noted Urgent treatment for symptomatic AAA
The key points of an AAA
Hyperaldosteronism: Conns Syndrome, adrenal adenoma, which does what?
Cushing’s Syndrome: hypercortisolism and HTN is one finding
Adrenocortical HTN
*secretes excessive aldosterone, hypokalemia and hypernatremia
Known as chronic pneumonia and caused by what?
The bacteria is slow growing and acid-fast bacilli
It is a cell-mediated immune response causing caseating necrosis, and cavitation. The macrophages ingests the bacilli, the pathogen resists killing so the macrophage present antigens to the T4 cell, which stimulates the macrophages to release the bacilli and lytic enzymes. This causes damage to the lungs. T8 cytotoxic cells develop in 3-6 weeks which can then kill the pathogen, a granuloma forms with central necrosis and walls off the infection in primary cases. The organism remains dormant and may reactivate.
Tuberculosis
*M. Tuberculosis
Aneurysm and rupture of the vessel wall: advanced vulnerable plaque weakens the vessel wall causing it to rupture with hemorrhage. Once the plaque has ruptured a thrombosis will occur over the plaque causing acute obstruction of the lumen, which will cause ischemia and or embolization later. The plaque and thrombosis will continue to grown until it reaches critical stenosis which causes the infarction or ischemia of the tissue.
The progression of plaque
Polymositis
SLE
Hypersensitivity Myocarditis
Non-infectious causes of myocarditis
Fibro-fatty lesion within the intima of the large and medium arteries. What is the leading cause of? This begins with a injury to the intima and the accumulation of lipids (extra and intra), proliferation of smooth muscle, scar tissue and calcification. Causes 50% of deaths in the USA Less common in Africa, South America, and Asia Risk factors are multiplicative: more risk factors the more likelihood of this occurring.
Atherosclerosis *Coronary artery disease, CVA, PVD
Breach in the vascular wall. Hematoma, between which two layers? Pulsating hematoma
Pseudo-aneurysm *media and adventitia
10 mmHg or more fall in SBP with inspiration
Usually the decrease in intrathoracic pressure that occurs during inspiration accelerates venous flow, increasing right atrial and right ventricular filling. This causes interventricular septum to bulge to the left producing a slight decrease in left ventricular filling, stroke volume output, and systolic blood pressure. In this case, the fluid in the pericardial sac produces further compression of the left ventricle, causing an exaggeration of the normal inspiratory decrease in stroke volume and systolic blood pressure.
Pulsus Pardoxus
Angina Pectoris: stable vs unstable
Acute Myocardial Infarction (STEMI or NSTEMI)
Chronis IHD
Sudden cardiac death
4 clinical syndromes of IHD
Pt comes in with fatigue, increased peripheral venous pressure, ascites, enlarged liver and spleen, distended jugular veins, weight gain and dependent edema. This may be secondary to chronic pulmonary problems. It appears that the RV is failing leading to congestion of venous and hepatic circulation, consequences of left-sided heart failure (What are less common etiologies?), peripheral edema, liver engorgement, GI tract congestion/ ascites (from what?) and elevated CVP and JVD.
RV Dysfunction
*Chronic lung disease or pulmonary HTN (severe), pulmonic stenosis or tricuspid regurgitation
*Anorexia and GI distress
Absolute goal of AMI is reperfusion ASAP and attempt the salvage the myocardium. However, reperfusion can cause problems via 4 mechanisms: mitochondrial dysfunction, myocyte hypercontracture, free radicals and leukocyte aggregation
Reperfusion Injury
This is the most common type of vasculitis. It is a chronic granulomatous inflammation. What are arteries that are commonly affected? There are definite signs of inflammation and increased sed. rate
Giant-Cell Arteritis *temporal artery, ophthalmic artery, and vertebral artery
True type Spherical Outpouching 5-20 cm Thrombi containing
Saccular Aneurysm
35-50% are genetic: 40 genes possible: AD inheritance, mutations in cytoskeleton proteins
ETOH abuse: can be other toxin induced
Doxorubicin (Adriamycin): chemotherapy
Hemochromatosis: Iron overload: can occur after pregnancy
SLE
Amyloidosis
Sarcoidosis
PAN
Peripartum
Myocarditis: infection
Causes of DCM
Reversible heart failure
reversible electrical aberrancy
Heart block, SVT, VT
Myocardial response to ischemia
Stunned myocardium
Plaque will cause ischemic bowel disease
Small intestine
>160/>100
Stage 2 hypertension
Infect the lung and lower airways in respiratory infection
Serious pneumonia (lung infections): this has a high potential for what?
Bacteria, fungi, mycobacterium, opportunistic
*morbidity and mortality
Attachment of pathogen to respiratory epithelium
Necrosis
Inflammatory response
Interstitial inflammation
Extends to alveoli: purulent exudate in alveoli
Agents: mycoplasma pneumoniae, Chlamydia, adenovirus, influenza, varicella, and measles
Usually causes low grade fever, headache, muscle aches, non-productive cough, dry hackling cough, and fatigue
Usually lasts 3-4 weeks
Pathophysiology of Atypical Pneumonia
A patient comes in presenting with ischemic skin changes, ulcerations, edema and poor wound healing on their legs. Embolisms are rare, especially in superficial veins. There are dark purple excoriations. You use a doppler to verify.
Venous Stasis Dermatitis
Results from another disorder such as renal disease
Secondary Hypertension
Accumulation of intracellular and extracellular lipids, SMC proliferation, scar tissue and calcification. Atherosclerosis plaque type
Fibrous plaque
Lipid SMC proliferation Scar tissue Calcification
What is fibrous atheromatous plaque composed of?
The chylomicron remanent is transferred to the liver where it is turned into VLDL released and then converted to IDL the LDL. The LDL is taken up by the endothelial cells and liver receptors and if these receptors become saturated then the scavenger receptors will take up the LDL depositing plaque in the vessel walls. The cholesterol is taken by the HDL and returned to the liver. HDL comes from the exogenous cycle
Endogenous pathway of cholesterol
Stable angina
Fixed narrowing and deficit of O2 supply, when demand is increased, transient ischemia occurs
Stable or fixed plaque
Starling Mechanism: increased EDV leads to what?
Sympathetic Nervous System: Increased HR and Contractility and blood is shunted to where?
RAS: AT2 and aldosterone are increased
ANP: elevated in this disease and released from what?
Myocardial hypertrophy and remodeling
CHF Compensation
*increased stretch and CO and myocardial O2 demands
*Brain and heart, away from skin, muscles and kidneys
*dilated aorta
Reactivation or re-infection with this disease
Often occurs during immune compromised
Cavitation of lung and bronchial dissemination occurs
Pt will present with cough, hemoptysis, fatigue, weight loss, dyspnea, and is a progressive illness
Reactivates in the apex of the lung: cavitary, necrotizing, chronic
Erosion into the bronchi
HIV co-infection: High risk for recurrence
Secondary TB
Atherosclerosis through the mechanism of plaque putting pressure on Media which is decreased from decreased perfusion. Where are the most common locations? Hypertension is the number two cause
The number one cause of AAA *abdominal, iliac, arch, and thoracic aorta
A patient comes in with encroachment of mediastinum, respiratory structures causing short of breath and dyspnea, compression of esophagus causing difficulty of swallowing,, persistent cough, chest pain, and aortic rupture shock. The patient also has pain straight through back.
Thoracic Aneurysm
Not present or incubating on admission to the hospital
>48 hours after admission
Ventilation, immunocompromised, COPD
Caused by what bugs?
HAP
*E.coli, Klebsiella, Staph, psuedomonas aeruginosa, Enterobacter
Endothelial dysfunction (list the process). Migration of monocytes and smooth muscle cells into the intima. Platelets and macrophages secrete what? The secretions stimulate smooth muscle cells to proliferate and to secrete collagen for the ECM. The ECM stabilizes the plaque and matures it.
Pathogenesis of atheroma *increased permeability, leukocyte adhesion, monocyte adhesion, and platelet adhesion *growth factors
Patient comes in with severe, crushing substernal chest pain. The patient says they are experiencing pressure and the pain has radiated to their left shoulder (where else can this radiate?). The pain is lasting 20 minutes to several hours. The pain is not relieved by nitroglycerin. The patient is experiencing diaphoresis, dyspnea, and nausea/vomiting. The patient’s pulse is rapid but could be weak as well. What is going on with the patient?
AMI
*neck and jaw
Disorders of the heart muscle: dysfunctional myocardial performance, which can be mechanical or electrical (heart failure vs arrhythmia)
There are two classifications: primary (confined to myocardium/genetic) vs secondary (associated with other diseases)
Due to intrinsic myocardial dysfunction due to genetic or other toxic or metabolic issues
Consequences of CV pathology places abnormal loads on the heart or causes ischemic injury of myocardium in which this results
Cardiomyopathy
Pt comes in with paroxysmal nocturnal dyspnea, elevated pulmonary capillary wedge pressure, cough, crackles, wheezing, blood tinged sputum, and tachypnea (pulmonary congestion). Restlessness, confusion, orthopnea, tachycardia, exertional dyspnea, fatigue and cyanosis. It appears the LV is failing. The pt has decreased CO and elevated pulmonary congestion. Filtration pressure in pulmonay capillaries exceeds osmotic pressure and pulmonary edema. The patient has a history of HTN and AMI whic are the most common causes of this. The pt is also experiencing aortic stenosis (what other valvular disease can this be?)
LV Dysfunciton
*Mitral regurgitation
140-59/90-99
Stage 1 hypertension
Inborn/ inherited risk
Race
Age-related
Metabolic syndrome
Blacks: earlier onset and more severe with complications
Insulin resistance: Type II Diabetes, hyperlipidemia
Primary HTN Risk factors
A patient comes in with “hardening of the arteries”. There is thickening of the arterial wall and a loss of elasticity. This is more diffuse and can lead to ischemia. It has affected only the small arteries and the arterioles. It is hyaline and hyperplastic. The patient also presents with hypertension and diabetes mellitus. You observe a widened pulse pressure (Which is?) What does the patient have?
Arteriosclerosis *High SBP and low Dbp
First there is injury to the endothelial (intima) injury: this is the initial step in plaque formation (monocytes and platelets stick to the injured lining) and endothelial cell dysfunction. Injury is induced by LDL, smoking, inflammation and HTN. Migration of inflammatory cells: move between endothelium into intima Smooth muscle proliferation Lipid accumulation Extracellular matrix (ECM) stabilizes plaque
Atherosclerosis Pathogenesis
Increases pulmonary blood flow and is not associated with cyanosis.
Exposes right side of the circuit to high pressure and volume to the left side.
This leads to what?
This causes injury to the lung capillaries in which the immune response causes collagen to build, hardening the vascular beds on the right side, building more pressure causing what? and right side heart failure
Left to right shunt
*RV Hypertrophy and pulmonary HTN.
*pulmonary hypertension
Function of 3 parameters:
Preload
Afterload
Myocardial contractility
Stroke Volume
Renal artery stenosis or atheroma
Glomerulonephritis
Chronic renal failure
Renin secreting tumor
Renal causes of Secondary Hypertension
Nephrosclerosis: chronic kidney disease, accelerates diabetic kidney disease
Dementia
Stroke/TIA
Retinopathy
PVD
Target Damage by HTN
This is formed within the intima which is deep to what? It contains a fibrous capsule which is composed of smooth muscle cells, macrophages, and collagen. There is a necrotic center, which contains what? There is also macrophages, lipid and cholesterol esters.
Plaque anatomy *endothelium *debris, cholesterol crystals, calcium, and foam cells
Plaque will cause renal failure and ATN
Kidneys
Blood splays apart the laminar planes of the media and forms a blood filled channel within the aorta wall. There are two main groups affected, who are they? There is degenerative medial changes with weakening of the tunica media. The intimal tear starts the process and then the pressure forces medial hematoma
Aortic Dissection *men age 40-60 with HTN and Marfan’s disease
Patient comes in with a severe headache, sub-arachnoid bleeding, and increased ICP. The patient has been asymptomatic until now. It appears to have affected the cerebral arteries. There are small spherical dilations at the point of bifurcation in the Circle of Willis.
Berry Aneurysm
Progressive primary or secondary
Disseminated: systemic symptoms
Multiple lesions in the liver, spleen, kidneys, meninges
Highly symptomatic
Miliary TB
Rapid loss of contractility
Electrical irritability: arrhytmia focus
Cell/mitochondrial swelling (dysfunction)
Progression: ischemia to infarction
Functional changes in the myocardium as a response to acute ischemia
95% of this is “essential” or secondary
chronic elevation in CO and/or SVR or both
Slow but progressive damage: kidneys- small arteries- PVD-Heart (LV hypertrophy)
Chronic Hypertension
Assess clinical severity of CHF
Cardiac structure
Cardiac Function
Etiology of heart failure
identify comorbidities ad exacerbating factors and barriers to treatment
Initial evaluation of Heart Failure
synthesized by the liver high in TG and some cholesterol carry TG to adipose and muscle cells what is left over? where does the conversion occur?
VLDL *LDL * in the vessels
During heart failure, the heart experiences compensatory dilation: dilating cardiomyopathy and new sacromeres are added. The heart also experiences compensatory hypertrophy causing what?
Requires more O2 and makes the heart vulernable to ischemia
Myocardial Structural Changes
*Thickened ventricle
Most myocytes exhibit hypertrophy rather than hyperplastic, with areas of replacement fibrosis and lesser hyperplasia with necrosis.
Big, boggy and weak heart muscle
Cardiogenic: due to stresses placed on the heart by CV disease, which causes the heart to become bigger and floppier
The heart needs to handle more blood than usual causing aortic regurgitation, mitral regurgitation, and pulmonic or tricuspid regurg.
Ischemia of the heart muscle over time leads to weakness of heart muscle and this disease due to chronic IHD.
DCM Pathology
Dietary: decrease caloric intake, lower saturated fats, and lower cholesterol. HMG-CoA Reductase: statins (what are these complications?), reduces/ blocks the enzymes that synthesize LDL cholesterol, and TG are also decreased.
How do you manage cholesterol? *liver toxicity and muscle breakdown
A patient comes in with distal swelling, redness, tenderness, and has a positive Horman’s Sign. You are concerned this clot will travel to where? This can start from the local injury to the vein or stasis and may be a hyper coagulation problem.
Deep femoral vein clot *lungs
Elderly patients
COPD and chronic bronchitis
cause of CAP
M. Catarrhalis
Acute myocardial infarction is 2x as high in patients with this disease Macrovascular vasculopathy and microvascular disease Marked increases in stroke and AMI 100 fold increase in atherosclerosis and gangrene of extremities
Diabetes Mellitus
Cushing’s
Pheochromocytoma
PIH
Endocrine causes of secondary HTN
Methionine derived (amino acid from protein breakdown) Inhibits “anticoagulant” cascade Damages endothelium
Homocysteine
Pt comes in complaining of facial pain, purulent nasal drainage, congestion, headache, fever, decreased smell, turbinate edema, and crusting. The pt has had the symptoms for 7 days and you tell the pt it can last up to 4 wks. The common cause of this is mixed viral and bacterial infections (what are the common bugs?). You prescribe the pt nasal corticosteroids, antibiotics, mucolytics, and decongestants.
Rhinosinusitis: Acute sinusitis
*Rhinovirus, S. pneumoniae, H. Flu, and M. catarrhils
Vasoconstrictors: increases SVR through what?
Vasodilators: decreases SVR through prostacyclin, bradykinin, nitrous oxide, and beta-adrenergic
Modulators of systemic vascular resistance
*Angiotension II, Catecholamines, thromboxane, leukotrienes, Endothelin-1, and alpha-adrenergic
Cyanotic anomaly and consists of pulmonary stenosis, VSD, RV hypertrophy and over-riding of the aorta.
Born with right to left shunt
mixing of venous and arterial blood
Most common cyanotic congenital heart disease
Diminished pulmonary blood flow creating a large right to left shunt
No pulmonary HTN and can be surgically corrected.
Tetralogy of Fallot
Neutropenia
DM
IV Drug users
Abnormal heart valves
Pacemakers
Risk factors of endocarditis
>140/>90 mmhg
Standard definition of hypertension
Most common heart anomaly
Most close in early childhood when the patient will appear asymptomatic.
If this doesn’t close it causes a left to right shunt, pulmonary HTN, CHF, and eventually the reversible of the shunt causing cyanosis.
VSD
Given off by the RCA and supplies the posterior wall of the heart, posterior septum, and the SA/AV nodes and posteriot papillary muscles
Posterior descending artery
Overt pulmonary edema
Cardiac enlargement
Chest radiography
Spontaneous, rapid, jerking, purposeless movements
Facial grimaces
Irritability with behavior problems
Chorea
240 is high
Total cholesterol levels
Vasospasm of coronary vessel
Vessel may be normal
this is caused by a coronary artery spasm, which may have occurred due to endothelial dysfunction, hyperactive sympathetic nervous system responses, defective handling of the calcium by vascular smooth muscle or an alteration in nitric oxide production. The spasms can be triggered by cold weather, stress, medications, smoking and cocaine use. Some patients may experience hypercontractility of vascular smooth muscle, migraine headaches, and even Raynauds phenomenon. This occurs usually during rest or minimal activity and during the night. On an EKG there will be transient changes such as ST elevation or depression, T-wave peaking, and inversion of the U waves. Drugs such as calcium antagonists and nitrates are used to help control the spasms.
Prinzmetals Angina
Plaque is disrupted and ruptures or hemorrhages. This exposes the vessel to collagen. The platelets will adhere here and aggregate, releasing mediators such as thromboxane. This will cause vasospasm and the coagulation cascade will being causing a thrombus which will occlude the lumen. Myocardial necrosis will occur.
Pathogenesis of AMI
Patient comes in with acute symptoms of a severe headache, visual changes (scotoma), renal failure, new onset of chest pain (IHD), thoracic aneurysm, acute focal neurological symptoms. About 5% of HTN presents in acute fashion
Rapid rise in BP: if untreated it can lead to death in one year
200-220/120-140: typically a very high DBP
Either superimposed or acute new onset
Malignant HTN
You are describing a new diagnosis that you believe the patient has. You tell the patient this disease is dependent on the specific vessels that are involved, whether it is coronary, renal or aorta, the degree or extent of obstruction, and the acuity of the vessel narrowing. You also tell the patient that the narrowing and ischemia can take two pathways. The first pathway is the progression of plaque narrowing to critical stenosis this is slow and cumulative. The second pathway is plaque injury with acute ischemia which will lead to what? What are you describing to the patient?
Atherosclerosis (clinical presentation) *Thrombosis, hemorrhage, aneurysm, or rupture
30-40% of AMI
Necrosis of the right ventricle
If Right side dominant the necrosis can also occur in the posterior 1/3 of the septum and posterior left ventricle and can lead to left ventricle ischemia
Right Coronary Artery occlusion
Pt comes in with abrupt onset of fever and rigors. Has a watery nasal discharge with headache.
Cough
Sore throat
Muscle aches
What does the patient have?
Clinical influenza
Altered form of LDL Independent risk factor for atheromatous formation Enhances cholesterol delivery to injured blood vessels Suppress Plasmin and promotes SM proliferation
Lipoprotein-a (Lp-a)
Anti-bodies bind to PMNs, which release reactive oxygen species, and these titers correlate with disease.
ANCA
Results in cyanosis: causing a blueness and dusty appearance of the skin
Pulmonary circulation is bypassed
De-oxygenated blood is mixed with oxygenated blood
Adequate perfusion with no ventilation
The venous blood is bypassing the lungs and oxygenation and results in venous admixing of blood and cyanosis.
Low O2 in blood and high CO2
Right to left shunt
Develops in previously unsensitized, unexposed persons: convert to a positive PPD skin test
Inhaling droplets containing the bacilli
95% develop the latent for: granuloma formation within the lung and spread is limited and non-infectious
5% develop primary progressive form: the immune response is inadequate due to HIV or an immunocompression causing fever, night sweats, weight loss, fatigue, and cough
Sputum is AFB positive
Primary TB
Perform a sputum exam: Gram-positive and PMNs
Blood culture: may be positive for GPC
Lobar or Bronchopneumonia
Aspiration: from nasopharynx
Lung abscess ot Empysema may form (1-2 wks after)
Sepsis may be secondary
CAP tests
Filling is restricted due to rigid ventricles
Diastolic dysfunction (similar to secondary HCM)
Idiopathic or secondary
Amyloidosis, sarcoidosis, radiation fibrosis, metastatic tumors, and MM
What symptoms appear?
Restrictive Cardiomyopathy
*Dyspnea, PND, Orthopnea, fatigue and weakness
Atherogenesis: plaque formation dur to endothelial damage: the high pressure damages the endothelium. What can this lead to?
Hypertensive-associated degenerative changes of the vessel walls: aortic dissection, cerebrovascular hemorrhage, and hyaline arteriosclerosis
The chronic pathological effects of primary HTN
* CAD, CVA, PVD
Starts in the subendocardial zone, which is highly susceptible to ischemia
Transmural necrosis occurs when the full thickness of the myocardium is affected and occurs 3-6 hours after prolonged ischemia without interuption
The intervention time is between what?
Irreversible damage as a response to ischemia
*onset and 6 hours
All acute IHD represents a sudden change in plaque distribution and thus myocardial ischemia with potential for infarction
Acute Coronary Syndrome
Necrotic myocytes begin to leak intracellular contents, such as enzymes that are normally ICF that leak into the interstitium and into the bloodstream
CK-MB
Troponin
Myoglobin
LDH
Which one is the first to show?
Which one stays elevated for weeks?
Which one peaks and levels?
Cardiac Biomarkers
*myoglobin
*LDH
*troponin
Large amount of blood or fluid
Constricts ventricular filling
Diastolic dysfunction
Decreased ventricular compliance
Cannot fill ventricle
Depresses cardiac output
Pulsus paradoxus
Pericardial Tamponade
Formation of vegetation on valves due to bacterial pathogens, which must have a portal of entry and can be due to bacteremia, staph (most common), Strep, haemophilus or oral microbes.
The aortic and mitral valves are the ones most commonly affected.
Endocarditis
Common cause of pneumonia in COPD pts or adults/children with chronic lung disease
H. Flu
Contractility is impaired
Decreased EF: 50%
Increased EDV and EDP
Increased preload
Dilates ventricle
Blood builds up in atria and pulmonary venous congestion and CVP
Systolic Heart Failure
Acute phase reactant (synthesized where?) Marker of systemic inflammation Predicts future CV disease or events Inflammation is etiologic in atherosclerosis
C-Reactive Protein (hs-CRP) *liver
The patient says the stabbing pain in the chest was a sudden onset. He is experiencing tamponade, aortic insufficiency, but not a myocardial infarction (yet). It appears to be involving the subclavian artery (what other artery?). You are concerned because the most common cause of death is the dissection into the pericardial, pleural, or peritoneal cavity. You must act fast, what does the patient have?
Thoracic Dissection *Carotid arteries (type A)
Small ones are tolerated well
Large or acute effusions create “tamponade”, which restricts the diastolic filling. The acute filling of 250 mL may disrupt ventricular filling and cause hemodynamic collaspe requiring acute pericardiocentesis
Inflammation may result in effusion >50 mL. What is the normal fluid amount?
There are two types
Serous: CHF
Trauma, malignancy, ruptured MI
Pericardial effusion
*30-50 mL
BNP: differentiates dyspnea form heart failure or lung disease ( 400 rule in)
Lab results for heart failure
A patient comes in with a history of chronic heart failure (what are the other risk factors?). It appears a clot has produced an inflammatory response. The clot is located in the venous sinus of the soles muscle, posterior to the tibia. The patient complains of calf pain, tenderness, and swelling. The patient presents with the triad, which is? You are concerned because the thrombosis can move causing more damage. This accounts for 95% of thrombophlebitis.
Deep Venous Thrombosis *neoplasia, pregnancy, obesity, post-op, immobilization, or OCP. *venous stasis, vessel injury, and hypercoagulation
Plaque progression to critical stenosis Plaque rupture and erosion (acute problem) Platelet adhesion and activation > thrombosis > partial or complete occlusion.
Pathophysiology of plaque
Thin fibrous cap Large lipid pool Less stenotic lesions Increase (ester/free) cholesterol
Factors that increase stress
Chronic VSD
Results in pulmonary HTN and increased pulmonary resistance
Reversal of shunt because now its right to left and causes cyanosis.
This is the progressive pathophysiology of chronic shunting.
The pulmonary vascular resistance will eventually succeed the systemic resistance causing the reversial of the shunt.
Eisenmenger’s Syndrome
Plaque ruptures acutely
Acute thrombosis of coronary artery, which develops ischemia
Caused by myocardial necrosis leading to heart muscle death, presence of biomarkers, or STEMI VS NSTEMI
What is the number one cause of this?
This is irreversible damage of the myocardium
1.5 million are affected per year and 1/3 die from the first event
10% before the age 40
50% before age 65
Acute Myocardial infarction
*atherosclerosis
there are 2 sites of lipoprotein synthesis (which are?) chylomicrons are synthesized in one (which one?) and transfer lipids (TG) into the adipose tissues and skeletal muscle via LPL Remnants (cholesterol) are transferred to the liver where synthesis of the VLDL occurs and is excreted in the bile.
Exogenous cholesterol pathway *small intestine and liver *small intestine
Plaque will cause CVA
Brain
fatal in days to weeks
occurs in young people
Giant Cell Myocarditis
Mitral stenosis
tricuspid valve stenosis
aortic regurgitation
tricuspid regurgitation
all cause what?
Disatolic Murmur
During heart failure, the sympathetic nervous system is stimulated. NE is released which increases what?
Renin-angiotensin system is activated and renin is released causing what?
Activation of Neuro-Hormonal axis
*contractility and heart rate
*salt and water retention and increased volume via elevated preload and higher filling ressures.
Infection: mycotic aneurysm Syphilis Vasculitis
Causes of Aneurysm
Obtain a fasting blood lipid profile The LDL is calculated via other lipid fractions (whats the equation?) This will result from any increase in the fraction Total cholesterol may be elevated by HDL or LDL Ratio of LDL/HDL is more important than TC
How to diagnose hypercholesterolemia *LDL= TC - HDL (TG/5)
Member of the herpes virus
Cytomegalic inclusion disease
Most common viral pathogen in AIDS pts
Pts present with pneumonitis, colitis, encephalitis, and retinitis
CMV
Viral or uremia
Shaggy
“Bread and butter”
Irregular surface
Fibrinous Percarditis
Pulmonary stenosis
Thickened right ventricle wall
Ventricular septal defect
Aortic overrides septal defect
TOF Elements
Patient comes in with progressive pain that is experienced with less exertion or at rest. The pain seems more prolonged or more frequent than pain from the patient’s past. The symptoms are less predictable and there has been a change in their angina patter. This is concerning because it could progress to necrosis/AMI. There has been a plaque disruption or instability. You perform an EKG and find ST depression, T-wave inversion, and NO ST elevation. You take a blood sample to test the enzymes and there is an elevation of enzymes so what does the patient have? If there were no enzymes present?
NSTEMI
*Unstable angina
Patient comes in with dyspnea, orthopena, edema, fatigue, and appears to clinically have heart failure.
Their ejection fraction is less than 40% (what is the normal?)
They appear to have a systolic heart pump failure
DCM
*50-75%
Patient comes in with a dilated and enlarged left ventricle. Tests demonstrate increased LV end diastolic volume and reduced or normal afterload. You hear a holosystolic murmur. Atrial fibrilation is also occurring. You hear at blowing at S1 and throughout the entire beat. What does the patient have?
Mitral valve regurgitation
Increased arteriolar resistance (vasoconstriction)
Increased SVR
Vascular changes involve functional vasoconstriction: cause of essential hypertension
60 high
HDL cholesterol levels
Contractile dysfunction: acute CHF and a flash of PE
Papillary muscle dysfunction: rupture: new murmur
Myocardial rupture: 3-7 days post infarction
Arrhythmias: heart block, SVT, VT, V.Fib
Pericarditis
Ventricular aneurysm
Complications of AMI
This is the inflammation and swelling of the MM of the nasal cavity and sinus lining due to the obstruction of the ostia. The anterior ethmoid, frontal, and maxillary sinuses all drain into what?
Acute, viral, allergic all may present in the same manner
Chronic may last 3-6 months with recurrence over time
What is the pathophysiology of this?
What is the cycle?
Rhinosinusitis
*osteomeatal complex
*there is an obstruction of the osteomeatal complex from a virus or allergen, which impairs mucociliary clearance. Polyps or barotrauma can also obstruct. Bacteria/virus grow in the sinuses and pus can form
Sinusitis triggers swelling which leads to blocked drainage which leads to stagnation and infection and back to swelling.
A patient comes in with intima injury. This results in smooth muscle cell and ECM proliferation. This is an inflammatory process and plaque is more focal causing narrowing. What does the patient have?
Atherosclerosis
Diets in high polyunsaturated fats, or low in total fats Omega-3 fatty acids Exercise Ethanol in moderation No obesity and cessation of smoking HMG co-ase inhibitors (class of drugs)
What causes a high HDL and low LDL?
Progressive dilation of chambers
Systolic dysfunction (contractile failure)
Heart is enlarged
Thinning and enlargement of all chambers
Most common form
Regardless of etiology: findings are similar
Impaired systolic function with heart failure
Dilated Cardiomyopathy (DCM)
High pressure left to right shunts
Loud systolic murmur
Leads to Eisenmenger’s if not corrected, so what will the pt experience
Patent Ductus Arteriosus
*cyanosis and pulmonary HTN
A patient comes in complaining of recurrent sinusitis, sore eyes, sore ear, stuffy nose, joint pain, and gangrene. The patient is running a fever and has purulent pansinusitis. The patient is coughing and has hemoptysis from pneumonia. They also present with hematuria and proteinuria. You describe to the patient they are experiencing necrotizing vasculitis that is affecting the respiratory tract in the sinuses, lungs, and kidneys. Autoantibodies are attacking proteinase 3. It is an ANCA. There is granuloma formations and patchy necrosis are in the arteries and veins. You can treat with anti-inflammatory drugs.
Wegener’s Granulomatosis
Narrowing distal to subclavian take-offs
Ejection of SV into narrowed aorta
High BP in upper extremities
Low BP in lower extremities
Coarctation of Aorta
There are two major mechanism of this and they are
acute pulmonary injury (which would be what?) and cardiogenic (which would be what?)
Pulmonary Edema
*ARDS, non-cardiogenic shock
*decreased contractility, high afterload, high preload, and diastolic dysfunction as well as a fluid overload.
As a child this patient presented with ventricular septum defect, pulmonary stenosis, hypertrophy of the right ventricle all overriding the aorta. Now as an adult the patient is suffering from pulmonary regurgitation, right side heart enlargement and tricuspid regurgiation.
TOF
Familial deposition is multi-factorial Related to hyperlipidemia (lipoprotein metabolism), hypertension, DM and what two others?
How are genetics non-modifiable risk factor of atherosclerosis? *CRP and homocysteine
A patient comes in complaining of ischemic pain, proximal swelling (this may not appear in other patients), pale extremities and leg is smaller than the other. They are experiencing hair loss and skin ulcers. This is not claudication so you can rule out?
Arterial Clot *a partial obstruction that is affected when exercising
Fever
Arthralgia
Prolonged PR interval
Increases ESR or CRP (sed. rate)
Leukocytosis
Must present with one major and two of these to be considered as what?
Minor Criteria for RF
*RF
Palpitations
Headache
Episodic sweating
Pheochromocytoma Triad
Infection follows aspiration of colonized upper airway (what is the most likely agent?)
Three groups are at risk ?
The bacteria adhere to the epithelium producing alveolar exudate, pus and edema fill the alveolus in lobar or patchy fashion. Interferes with O2/CO2 exchange
Purulent coough develops
Bacteremia is common
Sudden onset of severe rigors and fever
Malaise with fatigue and cough
Blood tinged sputum: Frank hemoptysis
Pleuritic chest pain
Progression to sepsis if not treated
CAP/ Typical Pneumonia Pathophysiology
*Immunocompromised, asplenic, chronic disease
Malignant
Shaggy, fibrinous exudate with blood
Fibrinous with bloody effusion
Major modifiable risk-factor of atherosclerosis Significant independent risk factor Elevated total cholesterol and LDL: marked increase in atheromatous formation. Usually expressed as lipidemia, high levels of lipids, dyslipidemia (uneven fraction of LDL and HDL) Usually an increase in LDL leads to an increase in total cholesterol
Hyperlipidemia
There is an imbalance of perfusion and myocardial oxygen demand
Ischemia will result from high oxygen demand (tachycardia) and diminshed oxygen supply leading to anemia, CO, obstructive plaque and thrombosis
Syndromes of myocardial ischemia
Coronary artery disease
Leading cause of death in the US
Ischemic heart disease
JVD
S3 gallop
Pulmonary crackles
Ascites
Edema
Laterally displaced apical impulse
Narrow pulse pressure
Tachycardia
Arrhythmia
Exam Findings of Heart Failure
Age Gender Family history Genetic abnormalities
What are the unmodifiable risk factors of atherosclerosis?
Saccular (most commonly occurs where?): a focal defect that appears sac like Fusiform is common in the aorta, entire circumference Ruptured Berry: congenital at bifurcation
The three forms of an aneurysm *brain
Toxoplasma gondii
Lyme disease (B.burgdorferi, conduction disorders, heart block)
Less common infectious etiologies of myocarditis
50% protein 20% cholesterol 5% triglycerides high in protein and phospholipids and low in cholesterol moves cholesterol from the vessel wall to the liver synthesized in the liver reverse transport of cholesterol from peripheral tissues and endothelium to the liver facilitates the clearance of cholesterol from atheromatous plaques and transports to the liver where is this excreted? higher levels correlate with reduced risk
HDL *in the bile
High intake of saturated fats and cholesterol (egg yolks, animal fats, and butter). Obesity Smoking
What will cause a high LDL and TC?
Most frequent cause of respiratory infections
Range from self-limiting to life threatening
Injure bronchial epithelium, obstruct airways and lead to secondary bacterial infection
What virus grows best at 33 degrees C and is isolated in the upper respiratory tract
What can infect both upper and lower resp. tracts?
Viruses
*Rhinovirus
*Influenza
A pt comes in with central obesity, high blood pressure, high TG, low HDL, and insulin resistant, what is their diagnosis?
Metabolic syndrome
cholesterol and triglycerides are insoluble in plasma. these are known as “transport proteins” that function to carry blood lipids. fats are less dense then proteins, so as the proportion of triglycerides decreases the density increases. The lowest density contains the greatest % of triglycerides, and the highest has the greatest % of protein
What is a lipoprotein
Affects all 3 walls. Saccular and fusiform Ventricular heart Congenital (Berry) Syphilitic
True aneurysm
A patient that is 55 years old comes in complaining of a fever, headache, diplopia and even some vision loss. The patient also complains of tenderness when you palpitate the temporal area. You order a biopsy and treat with corticosteroids. What does the patient have?
Temporal Arteritis
The plaque ruptures and the lipid core stimulates platelet aggregation. The platelets release mediators (which are?)
The glycoprotein receptors on the platelet membranes are activated (IIb/IIA)
Fibrinogen binds glycoprotein receptors on platelets forming bridges with ther aggregating platelets
Steps in thrombosis and Occlusion in ACS/AMI
*Thromboxane, ADP, thrombin
A patient comes in with a complaint of cosmetic problems. On the back of the legs it appears like dilated tortuous veins. This is due to prolonged increase in intraluminal pressure and is 10x the normal pressure. The patient complains of heaviness with standing and appears to have some edema. It appears the valves are incompetent causing stasis, congestion, edema, and thrombosis.
Varicose veins
Independent risk factor for atherosclerosis (systolic and diastolic) Increase risk of IHD/atherosclerosis of coronary arteries (CAD and ACS) (60% increase compared to normotensive) If left untreated 50% will die of IHD or CHF and 33% will die of a stroke (CVA) What is a major marker of this condition as a chronic condition?
Hypertension *LV hypertrophy
Secondary pneumonia after a viral infection
Frequent cause of lung abscess
Staph. Aureus
Fever and pulmonary infiltrate
Opportunistic microbes (?)
HIV pts, organ transplant pt, cancer treatment pt
Pneumonia in immunocompromised pt
*CMV, PCP, Candidiasis, cryptococcosis
A patient comes in with carditis, polyarthritism, chorea, subcutaneous nodules, and erythema marginatum. The patient has had a history of pharyngitis, fever, headache, and rash. These symtpoms are appearing of 2-3 weeks after the Group A symptoms. You perform exams and realize all 3 layers of the heart are inflammed (known as?). There is also valvular dysfunction which is a severe consequence. You explain to the pt that antibodies react with M-proteins of the GAS, these then cross-react with glycoproteins of the heart, joints, and skin. The patient may present with pancarditis, endocarditis, myocarditis, or pericarditis. You take a biopsy and examine Aschoff bodies.
Rheumatic Fever
*pancarditis
Orthomyxoviridae family or RNA viruses
Types A,B, and C
Type A is based on HA and NA surface glycoproteins, which are?
Both A and B can cause epidemics
Type C is less severe and causes respiratory s/s
An antigenic shift can occur due to changes in HA and NA
How does this spread?
How long is the incubation period?
Influenza
*H1-H5, N1-N9
*respiratory droplets
*1-4 days with a mean of 2 days
Occurs with a defect in the receptors causing high cholesterol and lipid levels at an early age, they have no HDL receptors so all go to the scavenger receptors.
Primary hyperlipidemia
Estrogen/Progesterone
Excess sodium and H20 Retention
Common cause of HTN in young women
Reversible after 3-4 months if stopped
OCP-induced HTN
A patient comes in with a sore throat, rhinorrhea, nasal congestion, cough, low-grade fever, malaise, fatigue and headache. You suspect a rhinovirus (what are the other etiologies?) You describe to the pt that the virus was transmitted from person to person via fingers to the nasal mucosa and conjunctiva. It can spread to surfaces and can survive for 5 hours. The particles can be aerosolized as well. The virus binds to the host plasma membrane receptors and cause inflammation. What is the incubation period? And how long are you contagious? Children are a major reservoir.
Common cold
*parainfluenza, RSV, Adenovirus, coronavirus
*4-5 days
*first 3 days after S/S
Plaque will cause CAD, Angina, STEMI, NSTEMI
Heart/ coronary arteries
Coarctation of aorta
hypervolemia
increased co
PAN
vasculitis
CV causes of HTN
Inadequate sodium excretion
Salt and water retention
Increased plasma and ECF volume
Increased cardiac output
New steady state of sodium: baseline is HTN
Defects in Renal sodium homeostasis: causes of essential hypertension
It is related to size: less than 4 cm is minimal risk 4-4.9 cm 1%/year 5-6 cm 11%/year >6 cm 25% 5 cm or more is managed aggressively It is likely that the patient has significant vascular disease elsewhere (?), increases the risk for what?
The risk of rupture for an AAA *heart, carotid, other major vessels *heart attack, stroke
A patient comes in with dyspnea, effort intolerance, orthopnea, PND, cough, edema, abdominal pain, and fatigue.
It appears the pts heart is failing to pump enough blood to meet metabolic demands, decreasing CO. The pt is using their cardiac reserve which is the ability of the heart to increase CO when needed during rest and when exerting energy.
Heart Failure
In heart failure, there is a decrease in CO, SV, and BP the preload then increases the stretch of the ventricle and increases CO. If the heart is unable to compensate congestion eventually results elevating Venous pressure causing symptoms to develop.
Starling Compensation
characterized by necrosis of the myocardial tissue and occurs due to atherosclerotic disease of the coronary arteries. This usually occurs with vulnerable plaque that ruptures and forms a thrombus, which creates an occlusion causing the acute myocardial infarction. The area in which this affects is based on the affected coronary vessel and its blood flow distribution. The full thickness of the myocardium is affected. S-T elevation, T-wave inversions and Q-waves are seen on an EKG. Signs and symptoms: abrupt onset of chest pain, which is severe, constricting, suffocating, and described as crushing. Pain can radiate to the left arm, neck, or jaw. Pain is prolonged and not relieved with rest or nitroglycerin dose. Fatigue, shortness of breathe, tachycardia, anxiety, and restlessness. Some patients complain of nausea and vomiting. Sudden death may also occur. Rapid treatment and identification is crucial to prevent the negative outcomes of this. A 12-lead EKG should be performed and oxygen, aspirin, nitrates, morphine, antiplatelet and anticoagulant therapy, beta-adrenergic blocking agents and ACE inhibitor.
STEMI
Type of atherosclerosis plaque Macrophages and SMC’s distended with lipid (very early lesion)
Fatty streak
Recurrent or severe
Fibrotic scarring, obliteration of space with dense fibrosis
Chronic or constrictive pericarditis
20% of AMI
Necrosis of the lateral left ventricle wall
10% is left dominant vasculature, there can also be necrosis of posterior 1/3 of septum and posterior left ventricle
Circumflex Occlusion
Plaque will cause PVD
Lower extremities
A femal patient comes in with a history of Marfan Syndrome (what other disease could it be?). It appears her floppy valve balloons into the LA during systole. The pt has chest pain, anxiety, palpitations, dyspnea, and a midsystolic click/ late systolic murmur which occurs between S1 and S2. What is a rare complication of this?
Mitral Valve Prolapse
*OI
*Infective endocarditis
A male patient who is suffering from Marfan’s has had a rupture into the peritoneal cavity below the renal arteries but above the bifurcation. The patient is suffering from ischemia from an obstruction of a branch vessel. The rupture appears to have been between 2-15 cm and there was abnormal collagen or elastic in the wall. You need to check for an embolus, impingement/compression or an abdominal mass.
AAA
is a clinical syndrome of myocardial infarction that can range from myocardial ischemia to a myocardial infarction. Biomarkers can be tested to determine this process. The biomarkers come from the degree of ischemia in the myocardium. This will occur when a partial occlusion of a major coronary artery or a complete occlusion of a small artery affected by atherosclerosis. This occurs when there is a rupture of the plaque and a clot forms which can partially occlude the artery and cause the heart muscle to become ischemic; however, only 1/3 of the inner myocardium is affected. The EKG pattern may demonstrate ST depression or T-wave inversion, no ST elevation, and no Q-waves “Non Q-wave infarct”. Patient will experience chest pain, difficulty breathing, nausea, vomiting, sweating, palpitation, and even cardiogenic shock if the affected area is a large area of the heart. A 12-lead EKG should be performed and oxygen, aspirin, nitrates, morphine, antiplatelet and anticoagulant therapy, beta-adrenergic blocking agents and ACE inhibitor
NSTEMI
Patient comes in with sharp, worse with movement chest pain. The patient says its relieved by sitting forward or sitting. You listen to their heart and hear a friction rub, which sounds leathery and is due to what? The EKG shows diffuse ST-T wave cahnges in all leads
Pericarditis
*Inflammed membranes
There is insufficiency or incompetence in this valve causing leaking of blood backward from the aorta to the LV. A diastolic murmur develops (after S2 before S1). It is an intrinsic valve disease like endocarditis. This is disruptive of the supporting structures such as the papillary muscles or the chordae tendonae: this usually occurs when?
Aortic valve regugitation
*After an MI
A patient comes in who has a history of HTN and is suffering from syncope, angina and developing CHF. It appears that the normal forward flow from the LV to the aorta is being prevented about 80-70% constriction. You explain to the patient that it is a process and the patient has experienced calcification which has developed into valve stenosis. You hear a systolic murmur. The patient has a decreased cardiac output because you hear a swooshing between S1 and S2. It appears flow has been diminshed to the coronary arteries. What is the most commonc cause of this? What are the 3 causes that of Ca build up? The patient is also experiecing LV hypertrophy because it is working to overcome the pressure of this disease. What other disease are these risk factors associated with? The surface area decreases from 4 cm to .5 cm or aortic annular increase in aortic transvalvular gradient of 7 mmHg with the reduction in effective orifice area of .1 cm squared.
Aortic Stenosis
*Calcific aortic stenosis
*Age, HTN, hyperlipidemia, and Inflammation
*atherosclerosis
Patchy distribution of inflammation: usually occurs in more than one lobe
Starts as bronchitis: spreads from the bronchioles and involves the alveoli: pus and fluid filled
Bacterial etiology is usually the case
bronchopneumonia
Supplies the left lateral wall
Circumflex artery
Obesity with high calorie intake Sedentary lifestyle High TG and saturated fats Diabetes mellitus Metabolic syndrome (combination of risk factors)
Risk factors for secondary hyperlipidemia
Trypanosoma Cruzi
Variant form of myocarditis: protozoan agent
10% die of fatal myocarditis due to arrhythmia or CHF
90% have 10 year immune mediated phase then experience progressive CHF and lethal arrhythmia
Chagas Disease
Loss of lung volume causing inadequate expansion
Results in shunting: inadequate oxygenation of pulmonary blood flow, there is a ventilation perfusion mismatch.
The collasped lung segment is not filled with O2 and the walls collaspe
Acelectasis
What are the three subtypes of atelectasis
Resorption
compression
contraction
The only irreversible formof atelectasis?
Contraction
Treatment of atelectasis can prevent what and or what?
Hypoxia
Infection
What parts of the lung does atelectasis affect?
Segement
Several segments
complete lobe
entire lung
This is an obstructive process in bronchi or bronchiole from a tumor/mass, mucus plug, foreign body, asthma, bronchiectasis.
It prevents the air from reaching distal alveoli
Resorption type of atelectasis
This is an accumulation of fluid, air, or blood in the pleural space.
There is a mechanical collaspe of the lung
Air would cause an pneumothorax
Blood would cause a hemothorax
Fluid would cause an effusion
Compression type atelectasis
This occurs when air accumulates in the pleural space.
Loss of negative pleural pressure because it equalizes with the atmopshere so the trans-thoracic pressure becomes 0 causing the lung to collaspe.
Pneumothorax
This causes fibrosis or scarring of part or all of the lung which hampers the expansion of the lung in a segement or the entire lung.
The scarring can be in the lung parenchyma or pleural membrane.
This is not reversible
It caused by radiation fibrosis and pulmonary fibrosis.
Contraction Atelectasis
Patient comes in with an acute onset of severe dyspnea, hypoxemia (low arterial O2), and pulmonary infiltrates (fluid accumulates in alveoli and pulmonary edema) from non-cardiogenic edema. Tachypnea with respiratory failure. Atelectasis, cynaosis and multi-organ failure (renal, GI, CNS). What does the pt have?
ARDS
What are the direct pulmonary causes of ARDS?
Pneumonia
Burn with inhalational injury
Near-drowning
aspiration
pulmonary contusion
pulmonary embolus
What are the indirect causes of ARDS?
Sepsis
Trauma/shock
Uremia
transfusion
Drug OD
Severe Pancreatitis
Diffuse epithelial cell injury causing damage to alveolar capillary membrane, which increases the permeability causing fluid, proteins, blood cells to move into the alveolus.
There is damage to type-2 cells, which cause a surfactant depletion, atelectasis and collaspe, shunting of the blood, impaired ags exchange from hyaline membrane and hypoxemia.
The lungs lose their diffusion capacity.
Pro-inflammation
What is this?
Pathology of ARDS
A newborn pt comes in and appears to have a newborn respiratory distress syndrome. The baby cannot make surfactant causing the alveoli to collaspe. There is inflammatory damage to the alveolar membrane and alveolar flooding. A hyaline membrane is formed making it difficult for O2 to diffuse across.
What does the patient have?
Hyaline Membrane Disease: Neonatal ARDS
This is a chronic and recurrent airflow obstruction
It is progressive and non-reversible
Airway hyperreactivity
4th leading cause of death in the US
85% of ppl with this are smokers or have been exposed during their job, silicosis, chronic infections, and CF.
There are two different forms: emphysema and chronic bronchitis
What disease is this?
COPD
Enlargement of air spaces distal to terminal bronchioles
Destruction of air spaces and alveolar walls
Loss of lung elasticity and dilated air sacs
Hyperinflation with air trapping
Increased TLC
What is this and what are two major causes?
Emphysema
*Smoking and Alpha antitrypsin deficiency
portion of the bronchiole tree distal to the terminal bronchiole
gas exchange occurs here
affected by emphysema causing destructive changes that dilate these permanently
consists of respiratory bronchioles, alveolar duct, and alveolus
What is this?
Acinus
This is a hereditary deficiency (1-2% of COPD)
15-20% of normal levels
This is an enzyme which inhibits elastase, a protease released by inflammatory cells (PMNs) which degrades the airways by breaking down elastin
Normally this is protective of the airways
This causes emphysema
Alpha-A antitrypsin Deficiency
Results in inflammatory cells moving into lungs
Release elastase degrading the airways
Decreases A1AT levels over time which inhibit elastase
Causes emphysema
Smoking
A pattern of emphysema
Central portions of the acini are affected
Distal aspects are spared and are normal and fully functional
Seen with chronic smoking but without A1AT Deficiency
Centriacinar Pattern
A pattern of emphysema
Acini are uniformly enlarged and dilated
more common in lower lung zones
More common in A1AT deficiency and smoking
more severe and worse prognosis
Panacinar pattern
What is the pathogenesis of emphysema
Toxic substances (smoke and polluntants) induce ongoing inflammation, which injures the epithelial cells and ECM breakdowns. Alpha 1 antitrypsin if present will help to prevent ongoing damage and induce repair.
A pt comes in with dyspnea that seems to be progressive. The pt is coughing and wheezing. The pt has experienced weight loss. After a test the pt has reduced FEV1 and FEV1/FVC. The pt is hyperventilating
appears like a pink puffer
this is an obstructive disease of the acini
dilation and dysfunction of alveoli and small airways
Emphysema
Excessive mucus production and plugging
Hyper responsive airways: bronchospasm
Constricted airways with cough which is productive and persistent (what is the criteria?).
Caused by smoke and pollution
Affects 25% of males
Chronic Bronchitis
*3 consecutive months in 2 consecutive years with purulent sputum
What is the pathophysiology of chronic bronchitis
The mucus secreting glands are enlarged, hypertrophic and there is an increase in globlet cells.
The bronchioles are also inflammed due to inflammatory infiltrate in the bronchiole walls.
The bronchioles spasm
Fibrosis of the bronchiole walls will occur
This is a protective response against smoke which results in airway damage.
You have a pt that presents with high CO2 and low O2. He looks like a blue bloater
Has cyanosis and progressive dyspnea with a cough
What does the pt have?
Chronic bronchitis
This is another obstructive airways disease.
It is intermittent and reversible.
There is obstruction of bronchioles (small airways) causing the airway to become inflammed increasing eosinophiles (eosinophilia). The smooth muscles of the bronchioles undergo hypertrophy. There is a spasm of the bronchioles and mucus is secreted into the airways causing an airway obstruction.
What is described above?
Asthma
This type of asthma is IgE mediated
Allergn sensitized
Most common type
Occurs in childhood
Type 1 hypersensitivity
Attacks are preceded by what?
Allergy induced
Similar to all RAD: reactive airway disease
Atopic/Extrinsic
*viral infection, antigen exposure, and urticaria/eczema
This type of asthma is triggered by URI, inhaled polluntants, irritants, exercise, and drug-induced
Eosinophil induced airways inflammation
Non-allergy related
not as likely to have a family history
aspirin ingestion
emotional upset
Non-atopic/intrinsic
A child comes in with a chronic cough that worsens at night, chest tightness, wheezing and dyspnea.
The child has airway inflammation causing edema and swelling as well as high resistance. They are hypersecreting mucus, having bronchospasms and air is being trapped in the alveoli.
FEV1 is decreased, peak flow is decreased, residual volume increases, increased work of breathing, mismatch of ventilation and perfusion, hypoxemia, pulmonary vascular resistance increases and expiratory wheezing, cough, dyspnea, and fatigue.
What does the pt have and how would you treat it?
Asthma
*B-2 agonist and corticosteroids
What is the pathogenesis of asthma?
Exaggerated hypersensitivity response to a stimuli
Both inflammatory cells and epithelial damage occur.
Hypersecretion of mucus, smooth muscle hypertrophy, and blood vessel proliferation
Overlaps between extrinsic and intrinsic OCCURS
This is permanent dilation of bronchi and bronchioles causing destruction of muscle and connective tissues. There is a cycle of inflammation and infection.
This is a secondary obstructive lung disease
The dilated bronchi and bronchioles are filled with mucus and dilated
Results from what?
Bronchiectasis
*Chronic infections, COPD, TB, Toxin exposure and necrotizing pneumonia.
A pt comes in with a chronic cough, dyspnea, and mucopurulent expectoration and foul smelling sputum.
The pt has had recurrent pulmonary infections which have been persisten and onstructive, usually from resistant bacteria/ polymicrobial
This may coexist with other chronic pulmonary diseases such as COPD
What does the pt have?
Bronchiectasis.
Patient suffers from hemoptysis, anemia, and diffusion of pulmonary infiltrates. Also hematuria, hypoxia, respiratory failure. A blood test illustrates IgE antibodies. This is a type 2 hypersensitivity reaction so the antibodies are directed against alpha three chain of collagen type 4 in the alveolar wall and glomerular membrane.
This is a primary immune-mediated disease. The pulmonary infiltrates will diffuse parenchymal and interstitial consolidation and infiltrates. This results from immune mediated injury to the alveolar wall presents with interstitial pneumonia.
The pt also suffers from microcytic anemia and coughs up frank blood.
Glomerulonephritis and hemorrhagic pneumonia
What does the pt have?
Diffuse-Alveolar Hemorrhage Syndromes (DAHS) or Good Pastures Disease
Pt comes in with dyspnea, fatigue, syncope, right sided heart failure, and rv hypertrophy. It appears there is abnormal elevation of pressure within pulmonary arterial circulation. This disease is self-perpetuation: introduces secondary structural abnormalities causing smooth muscle proliferations, fibrosis, and intima proliferation. It can be primary or secondary. It is most likely this pt has secondary.
What does the pt have?
Pulmonary hypertension
What are the 4 major mechanisms of pulmonary HTN
Elevated pulmonary venous pressure: diastolic dysfunction or MR
Increased pulmonary blood flow: left to right shunt with VSD
Pulmonary vascular obstruction: pulmonary embolus
Chronic hypoxemia: pulmonary vessels constrict with CO2 or low O2: COPD or chronic lung disease
This is a blood clot occluding a pulmonary artery
95% originate in deep veins of the lower extremities (what vein or above?)
Causes 50,000 deaths/year
60-70% are clinically silent
5% results in large “saddle emboli”
30% cause pulmonary infarct and symptoms of this disease. There is an lung infarction.
Pulmonary Embolus
*Popliteal
What are the risk factors for a PE?
Bed rest/immobilization
surgery
trauma/fractures
burns
CHF
Female/OCP/estrogen
Venous injury
Cancer/malignancy
Hypercoagulation
What is the pathophysiology of PE?
A thrombus originates in the vein in a deep venous system. The clincal outcome depends on the size, acuity of the process, and the size of segement of lung affected. There are two consequences: increase PA pressure: blood flow back to PA causing vasospasm and the release of mediators OR the ischemia of lung tissue later.
A sudden and marked increase in PA pressure causing a diminished CO
Right side CHF and could result in sudden death
Massive PE
Large occlusion: saddle PE
Pt comes in with dyspnea, chest pain, apprehension, cough, hemoptysis, sweating, syncope, palpitations, wheezing, leg pain/swelling
What does the pt have?
PE
Affects the lower lobes
Wedge shaped
Coagulative necrosis
15-20% of all PE
what is the most common symptom and what is this?
Pulmonary infarction
*dyspnea
This is fibrosis of the interstitium, which is composed of a basement membrane connective tissue between epithelium.
The fibrosis causes reduced compliance so it takes a higher pressure to expand the lungs, more work for breathing.
Usually has a normal FEV1/FVC
Hypoxia occurs
What is described?
Restrictive Lung Disease
What are the 4 types of restrictive lung disease?
Fibrosing disease
Granulomatous Disease
Eosinophilic disease
Smoking related
Patchy and progressive bilateral interstitial fibrosis which leads to decreased compliance and diminshed gas exchange across the fibrotic membrane. This leads to hypoxia, cyanosis and the cause is unknown (idiopathic)
What is this?
Idiopathic Pulmonary Fibrosis
What is the pathogenesis of IPF?
Repeated cycles of epithelial injury by an uncertain agent
There is abnormal repair which results in over-exuberant scarring and excessive fibrosis .
Excessive collagen is deposited in the interstitium
A pt in the hospital has developed later symtpoms of this disease which are severe dyspnea, worsening cough, and O2 dependent hypoxemia. This is a poor prognosis.
Earlier symptoms were dyspnea, cough and mild hypoxemia.
What does the pt have?
IPF
A pt has an onset of dyspnea, cough, and organizing pneumonia with an uncertain cause.
This appear to be a combination of chronic pneumonia and progressive pulmonary fibrosis causing injury from inflammation with infection and scarring.
What does the pt have?
Bronchiolitis Obliterans Organizing Pneumonia (BOOP)
This is caused by inhalation of particulate matter which can be coal dust, silica, and asbestosis. The particulate matter has to be between 1-5 microns where it can get lodged in smaller airways. This causes fibrosis and scarring to occur secondary to a reaction to the particles.
What is this disease?
Pneumoconiosis
This is the most common occupational disease from sandblasting or mining. The particles interact with the epithelial cells and macrophages, which release mediators (which ones?). This leads to inflammation and fibrosis. This is a restrictive lung disease. What is it?
Silicosis
*TNF, IL-1 and Fibronectin
What are the 6 disease processes related to occupational exposure of abestosis?
Interstitial fibrosis
Plaques on pleural membrane
PLeural Effusion
Lung carcinoma
Pleural malignancy: mesothelioma
Laryngeal cancer
PT comes in with gradual respiratory symptoms which consist of dyspnea, cough, chest pain. The pt also has night sweats, fever, fatigue, and weight loss. There is no caseating granuloma in the lungs and other organs. The course of this disease is unpredictable. It can be chronic disease, it can be resolved or progressive into restrictive lung disease/ pulmonary fibrosis.
What does the pt have?
Sarcoidosis
This is a restrictive lung disease and part of a multi-system disease. A non-caseating granuloma forms and causes scarring in the lungs and other organs. There is bilateral hilar lymphadenopathy leading to lung fibrosis. There is hilar adenopathy. Fibrosis/scarring and pneumonitis with adenopathy. There can be eye involvement with iritis, skin rash, and the liver and spleen can be affected. What is this?
Sarcoidosis
This is an immunologically-mediated inflammatory disease of the lung and results in allergic alveolitis. Usually occupationally related exposure to an antigen and unlike asthma there is bronchial inflammation. This is an immunological target of the alveoli and the interstitium between the alveoli. This is alveolitis, which is inflammation and fibrosis of the alveolar walls. THe bodies immune response to chronic exposure of an antigen. What is this?
Hypersensitivity Pneumonitis.
What are the findings of Hypersensitivity pneumonitis?
Findings describe a common immune-mediated mechanism/ pathology for all forms.
Increase in t4/t8 cells in the lung lavage specimens
Type 3 and Type 4 immune hypersensitivity
Non caseating granuloma formation in 2/3 of the pts
Interstitial patchy inflammation
Alveolitis
What are the syndromes of Hypersensitivity pneumonitis?
Farmers lung: moldy hay, M.faeni
Maple Bark Disease: moldy maple bark, cryptostroma carticale
Humidifer’s lung: cool mist humidifier: actinomycetes species
Pigeon Breeder’s lung: pigeons: proteins in the droppings
Pt comes in with fever, cough, dyspnea, and malaise 4-8 hours after exposure to the antigen
What is this?
Acute hypersensitivity pneumonitis
Pt comes in with insidious and indolent onset of cough, dyspnea and weight loss
What does the pt have?
Chronic hypersensitivity pneumonitis
Localized supprative necrosis in the pulmonary parenchyma. Cavitations. Necrotizing pneumonia. And can be 1-6 cm.
Aspiration of infective material, either orally or via gastric contents caused by what bugs?
Can be lung cancer with obstruction or a septic embolism
It can be a mixed infection with anaerobes.
Lung abscess
*Staph aureus, klebsiella, pseudomonas
Pt comes in with spiking fever with copious foul smelling sputum. Purulent sputum mixed with blood, malaise with fatigue, clubbing, anemia, and weight loss. What do they have?
Lung Abscess
What are the 4 major histology types of lung cancer?
Small cell
Adenocarcinoma
Squamous cell
Large cell
95% are carcinomas
5% are miscellaneous: carcinoid, fibrosarcoma, and leiomyoma.
It is metastic from breast, colon and liver.
Can be benign: hamartoma
5 Year survival: 16% of all types, 45% for causes localized to the small cell lung only
Peaks btn 50-60 yos
Lung carcinoma
What is the pathogenesis of lung cancer?
There is a stepwise accumulation of genetic abnormalities which results in the transformation of bronchogenic epithelium into neoplastic tissue. There are molecular changes which causes the inactivation of tumor supressor genes (chromosome 3), activation of KRAS oncogene and additional mutations which transform the epithelium into cancer. There are also dysplastic changes which is the progression of CIN1-3 > CIS, definitely present in squamous cell, this is a gradual process to malignancy
What is the progression of lung cancer?
Normal epithelium >> basal cell hyperplasia >> squamous metaplasia >> squamous dysplasia >> squamous carcinoma in situ >> invasive carcinoma
This type of lung cancer is greater in men than women
Arise centrally in the lung spreads to local hilar nodes
Central necrosis and cavitation
progresses to CIS and invasive cancer
Closely related to smoking
May be diagnosed early: dyspnea and CIS
What is this?
Squamous Cell lung cancer
This type of cancer usually start as peripheral lesions that may occur centrally and may arise in previous scars: scar carcinoma
Most common in women and non smokers
Atypical adenomatous hyperplasia: early progression before
AIS: atypical adenomatous hyperplasia>>cancer in situ
Slow growing
mestastize greatly, but slow growing
most common primary lung cancer, what is it?
Adenocarcinoma
This is a precursor lesion of cancer
glandular epithelium
progress to AIS> cancer
Atypical adenomatous hyperplasia
This is an undifferentiated malignant epithelium tumors of the lungs
Large nuclei and much cytoplasm
It is poorly understood : may present adenocarcinoma or squamous cell cancers that are poorly differentiated, usually agressive and early metastatic
What cancer is this?
Large Cell Lung Cancer
This type of cancer has centrally located masses with extension into the lung parenchyma, hilar nodes, and mediastinal nodes
Necrosis is present and extensive.
Derived from neuroendocrine cells of the lungs.
Associated with paraneoplastic syndromes
Invariable metastatic spread at the time of diagnosis: aggressive behavior, median survival is one year, not surgically resectable, and treated with chemo and radiation.
What is this?
Small cell lung cancer
What are the most common paraneoplastic syndromes associated with lung cancer?
Hypercalcemia, ADH, ACTH, and clubbing
A pt comes in with hoarness, chest pain, cough, hemoptysis, and superior vena cava syndrome. There is not neurological changes, so it hasn’t spread to the brain, there is hepatomegaly so it has spread where? No pain in the bones so it hasn’t spread to the bone and the pt doesn’t present with Addison’s so it hasn’t affected the adrenals.
What does the pt have?
Lung cancer
This occurs with lung cancer of the lung. There is obstruction and pressure on the brachial plexus, subclavian vessels, and presents with horner’s syndrome. What is horner’s syndrome and what is this?
Pancoast’s Syndrome
*Ipsilateral: ptosis, miosis, and anhidrosis.
