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Patho: Focus 5:

Terms in this set (84)

Hypertension
Sustained increase in peripheral resistance (vasoconstriction) or increase in circulating blood vol.
Overactivity of the sympathetic nervous system
Increase in peripheral resistance (vasocontriction)
Overactivity of the RAAS
Increase in peripheral resistance (vasoconstriction) and increase in blood volume.
Sustained release of Angiotensin-II
Increases in peripheral resistance (vasoconstriction)
Sustained release aldosterone
Increase blood volume
Stable angina
Plaque not ruptured. The plaque prevents artery from delivering more O2.
Pain occurs with exertion and relieved at rest
Instable angina
Cholesterol has Ruptured plaque and Pain will occur at rest
Myocardial Infarction
Ruptured plaque with clot information
Cardiac muscle dies within 20 minutes
Most risk factors for CAD to least
1.High LDL cholesterol, triglycerides, and HTN
2. African male with DM
3.Family with Hx heart attack, high LDL, and smokes
4.white female with elevated LDL cholesterol
5.white female exercise daily has HTN
A full thickness infarction or transmural infarction
Three muscle layers of the heart have died. The ECG shows an elevated St segment and called STEMI
Partial thickness infarction or subendocardial infarction
One layer of the heart muscle has died. The ECG shows ST depression and T wave inversion (- deflection) called NON-STEMI
Hx of symptoms
helps determine if the symptoms are consistent with a MI and if certain treatment can be given based on the duration of symptoms
ECG
Determines the type of infarction (Full/ partial thickness or STEMI/ NON-STEMI) and location.
Troponin
cardiac marker, only from the heart
males and females can have symptoms
chest pain, shortness of breath, nausea and vomiting, dizziness, loss of consciousness, and sweating; however, females have dizziness, loss of consciousness, and nausea and vomiting more often than males.
Peripheral neuropathy or damage to the peripheral nerves
Damage to the blood vessels supplying nutrients to the nerves from long-standing diabetes.
The autonomic nerves can be affected and if the ones in the chest are affected, the patient will not feel the pain even when the heart muscle is dying.
Aspirin for MI
Prevents clot from enlarging; decrease mortality significantly
Thrombolytic
Breaks up/down the clot/ must be given within 2hrs of symptom onset
Morphine
Decreases pain and anxiety
Beta Blockers
Decrease HR and contractility; thereby reducing O2 demand
Nitrates
Vasodilate coronary arteries to increase blood flow
Heparin/ warfarin
Prevent the clot from enlarging and prevent new clots form forming
Statins
lower cholesterol
Treatment of MI:
Coronary angiogram
-Dye injected into coronary vessels
-Shows where and how bad the vessel is obstructed-
Coronary artery bypass graft (CABG)
-Used only for triple vessel disease or worse
-Blood rerouted around plaque (at least 3 coronary arteries are occluded)-
Percutaneous coronary intervention (PCI)
-Angioplasty
-Balloon inflated to open vessel obstructed by plaque
-Stent may be paced to keep vessel open
Systolic HF
-Pump problem
-The heart muscle are small, thin, weak causing a decreased ability to contract
-Enlarged ventricle chamber
Diastolic HF
-Filling problem
-The cardiac muscles of the ventricles are enlarged causing Less space in the ventricle for blood
Left HF
Blood pump backs up into lungs causing Lung/pulmonary congestion
Right HF
Blood backs up into body causing swelling (edema) in the feet, legs, and abdomen.
Stroke Volume (SV) decreases
CO is decreased
HR decreases
CO is decreased.
Stimulation of sympathetic NS (compensatory mechanisms in HF)
Increases HR and SV (more forceful contract more/ increased contractility)
Release of ADH
Increases SV by filling up the ventricles so they contract more forcefully
Release of aldosterone
Increases SV by filling up the ventricles so they contract more forcefully
Myocardial hypertrophy
Increases SV by contracting more forcefully
Systolic HF causes
-Cardiomyopathy
-MI
-Valve diseases, (mitrial regurgitation /aortic stenosis)
-Dysrhythmias
-Eject infarction in systolic HF is low (less 40%). Normal ejection infarction = 55-70% of the blood ac contraction
Diastolic HF causes
-Chronic HTN
-Valve diseases e, aortic stenosis
-cardiomyopathy
Cardiomyopathy:
S/S due to decreased blood flow to lungs (Right HF)
-Right Ventricle isn't pumping enough blood to the lung causes = SOB and Increases RR.

- The blood back up into the body from the R VENTRICLE, will cause EDEMA of the legs, feet, abdomen
S/S due to decreased blood flow to body (Left HF)
-Left ventricle isn't pump enough blood forward to the body causing = Increased HR, Weakness and fatigue, and angina, fainting (syncope).

-Blood back up into the lungs causing = Pulmonary edema (fluid in the alveoli/ crackles sound).
Dilated Cardiomyopathy
-The heart chambers are enlarged
-CXR shows cardiomegaly
-Ejection fraction is decreased less than 40%
-Genetic, Viral (inflammation), Toxin (EOH), Pregnancy, Idiopathic (Unknown cause)
Restrictive Cardiomyopathy
-The heart is stiff and scarred causing smaller chambers (heart can't relax)
-Ejection fraction is normal and Blood backs up causing Pulmonary congestion shows in CXR heart side normal
-Caused by radiation to chest.
Hypertrophic Cardiomyopathy
-The cardiac muscle is enlarged in the septum which causes the heart chambers smaller.
-CXR shows normal
-Systolic ejection murmur increased with valsava -All children should be screened for this type
-Can causes dyspnea, syncope, or sudden death -Heart chambers small due to ventricular wall enlargement.
heart murmurs are caused by
an abnormal sound from the heart produced by turbulent blood flow through the valves.
A Functional Murmurs caused by
Increased blood flow through a normal valve in the heart
Pathologic murmurs caused by
Abnormal valves
Stenosis murmurs caused by
The valve is tight or stenotic and can't open fully to allow adequate blood flow thru the valve.
Regurgitation murmurs caused by
Leaky valve that doesn't close fully and blood backs up through the valve.
Mitral stenosis of valve disease
Problem with blood flows from l the left atrium to left ventricle
Mitral regurgitation
Blood backs up from the Left ventricle to the left Atrium
Aortic stenosis
Problem with blood flows from the Left ventricle to the Aorta
Aorta Regurgitation
Problem with blood backs up from the Aorta to the Left ventricle.
Mitral regurgitation from Rheumatic fever
A bacterial infection (Strepto) that causes joint pain, skin rash, and heart murmur, sob, fatigue, crackles
Mitral regurgitation from Rheumatic heart disease (RHD)
A condition is resulting from rheumatic fever, commonly causing from the heart valves are damaged (echocardiogram shows papillary dysfunc)
Mitral stenosis from Endocarditis
-Can infect a normal heart valve
-During dental work, bacteria can enter the bloodstream and cause an infection of a damage valve.
Aortic stenosis from age-related calcification
-Risk factor from smoking, HTN, high cholesterol, and DM.
-Anemia b/c RBC are broken. Syncope b/c not enough blood ejects out from aorta to the brain, -Chest pain = decreases blood flow to coronary arteries (hypertrophy)
Aortic regurgitation
Marfan's Syndrome, lung clear, fatigue, syncope, heart murmur, Pulse pressure Widened (increasing BP)
Abnormal Aortic Aneurysm (AAA)
-An intact abdominal aortic aneurysm (AAA) will present as constant abdominal pain radiating to the sides, groin, and lower back. A pulsatile abdominal mass will be felt. The most common site of AAA is right below the renal arteries.

-A ruptured AAA as much more severe abdominal pain with hypotension, tachycardia, syncope, and hypovolemic shocK, increasing BP
Complication of AAA
Clots, Compression of nearby structures, Pain, and Rupture.
Risk factors of AAA
Atherosclerosis, Age over 65 yrs, COPD, Family Hx, HTN, Male, and Smoking.
neurogenic shock
-Causes underactivity of the sympathetic NS and overactivity of the parasympathetic NS leading to low BP and HR, Warm SKIN
-Treatment: ATROPINE increases HR
cardiogenic shock
-Fluid overload occurs with elevated capillary wedge pressure (PCWP), and decreased cardiac index.Blood pressure 72/50
-S/S= JDV distended, Skin cool and Clammy from vasoconstriction
-Treatment= careful use of IV fluids
septic shock
-Occurs when the SIRS has been met, confirmed infection, bacterial infection has decreased urine output. Blood pressure 68/46; HR> 90; RR>20; temp above 100.5 or below 96.8F. WBC> 15k or <4K, and elevated lactate level. Blood pressure not responding to IV fluids.
-Antibiotics given.
anaphylactic shock
-Severe allergic reaction.
-S/S= presents with wheezing after a bee sting. Skin Flushed, SWELLING and ITCHING., BP 74/50; HR 132; RR 26; temp 98.2 F.
-Treatment= IV fluids, antihistamine (epinephrine given for hypotension and bronchospasm).
hypovolemic shock
-Shock resulting from blood or fluid loss
history of heavy alcohol use has liver failure with ascites. Skin is pale, cool and clammy; mouth and tongue dry. BP 78/52; HR 124; RR 16; temp 98.2 F. Elevated lactate level.
-IV fluids and pressors given.
Common all Shocks
Hypotension and give pressors (Epinepherine), decrease O2 delivery, Elevated lactate, Decrease perfusion
Focus: Renal System and UT Function
...
Cytistis
indicates infection/inflammation of the bladder.
SS= suprapubid/lower back pain
pyelonephritis (acute/chronic)
infection or inflammation of the nephrons of the kidney
SS= Costovertebral tenderness, Fever/chill, Flank/groin pain, and HTN
Cystitis and pyelonephritis
frequency and dysuria
Acute Kidney injury
-Decreased GFR
-Decreased Urine output or olguria
-Increased Nitrogen waste in the blood (Urea and creatinine called Azotemia
Prerenal AKI
-Reduced renal artery blood flow (↓blood flow to kidneys)
-Causes: Hemorrhage, vomiting, diarrhea, burn, sepsis, anaphylaxis, and cardiogenic shock.
Intrarenal AKI
-Direct damage to inside of the kidney(glomerulus /the tubules)
--Causes: Drugs (aminoglycosides), Myoglobin (muscle breakdown), Uric acid from cancer treatment, and Hgb from many RBC breakdown
Postrenal AKI
-Occurs with urinary tract obstructions: Ureters, bladder, or urethra
-Causes: Renal calculi (stones), Strictures (in the ureter/urethra), Tumors (kinking the ureter/urethra), Neurogenic bladder (bladder doesn't contract and empty after a spinal injury), BPH (enlarged prostate encroaching upon the urethra).
Stage 1 of chronic disease
Has some damage to the kidney
SS= Normal BP, normal BUN, normal creatine and GFR, and Protein in urine
Stage2 and Stage 3
-The GFR declines below 90 ml/min
-The blood pressure, BUN, and creatinine elevate.
Stage 4 and Stage 5
Further decline of the GFR,
Severe: increase BP, BUN, and Creatinine. Kidney loss func and filters the blood results in anemia, elevated Phosphate, Hyperkalemia, and metabolic acidosis. Stage 5 chronic RF with a GFR less than 15ml/min.
Anemia
-Caused by the kidney not secreting erythropoetin when the oxygen level in the blood is low (loss of secretion of erythropoetin)
-The red blood cells don't live as long when the toxins are in the body from kidney failure.
TREATED with packed RBC transfusion
Metabolic acidosis causes/treatment
- Occurs because the kidney is unable to excrete hydrogen and reabsorb bicarbonate.

TREATED sodium bicarbonate when the bicarbonate level is less than 15. Normal is 22-26.
Bone Fracture cause and treatment
-Inability to synthesize Vitamin D
-Inability to excrete phosphate
TREATED with phosphate binder
Hyperkalemia causes/ treaments
-the heart to be irritable so treatment is necessary to avoid dysrhythmias.
Insulin drives the potassium out of the blood and into the cell which buys time until the potassium can be excreted.

TREATED with CA and kayexelate
TREATED with Insulin and glucose
gouty arthritis (gout)
-The kidney's inability to excrete uric acid leading blood levels of uric acid increase, uric acid crystals deposit in the joints
CAUSES: swelling and pain.
TREATED with medications to decrease the synthesis of uric acid. However, medications to increase the kidney's excretion of uric acid will be ineffective.
Peripheral neuropathy
Peripheral nerves are damaged by the toxins in the blood.
Loss of feeling will occur commonly in the extremities/feet (sensory nerves damaged). Weakness or paralysis (motor damaged). Orthostatic hypotension (autonomic nerves damaged). BP drops causing lightheadedness and dizziness.
Changes in immune response
-Significant increase in WBC count doesn't occur with infection
-Significant rise in Temp doesn't occur with infection
-Loss of function and numbers of leukocytes
-Infection causes tachycardia, fatigue, ad slight temperature.
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