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
