Patho Exam 3

patho

Triad of Virchow: Venous stasis

\-factors that promote deep vein thrombosis

\-lack of movement, blood pooling, increased risk for clot

Triad of Virchow: hypercoagulable state

\-disease/condition that increases risk (cancer, bc pills, pregnancy, testosterone)

Triad of Virchow: venous endothelial damage

increases BP and blood sugar, surgery on major vein

hypertension 

\-elevated systolic (top), diastolic (bottom), or both    \[140/90\]

hypertension: modifiable

\-family history, older age, obesity, glucose intolerance (diabetes), low socioeconomic status (stress, and cortisol), smoking, increased sodium intake

hypertension: unmodifiable

\-myocardial infarctions, cardiovascular muscle hypertrophy, heart failure, kidney disease (glomerulus), and cerebrovascular accidents

orthostatic hypotension

\-compensation for moving from laying down to sitting up or sitting up to standing up. Is to increase the heart rate and vasoconstrict arterioles to raise BP.

\-failure to do this leads to orthostatic hypotension (postural hypotension) bc lower extremities don’t vasoconstrict

causes of orthostatic hypotension

\-antihypertensive drugs, altered body chemistry, prolonged immobility illness, volume depletion, venous pooling (pregnancy and lower extremity varicose veins

\-thromboembolic embolism

\-Deep vein thrombosis (large veins)

\-cardiac thrombi (valvular diseases, endocarditis, heart failure, atrial fibrillation)

air embolism

\-from injecting air through central lines or IVs which can cause stroke and heart attacks 

fat emboli

\-from long bone fractures which release fat into the blood stream. Trauma

venous emboli

\-can travel to the lungs = pulmonary embolus 

cardiac emboli

\-can travel to the brain =thromboembolic cerebrovascular accident 

\-travel to the cardiac vessels = myocardial infarction

coronary artery disease (CAD)

vascular disorder that narrows coronary arteries (atherosclerosis)

\-results in imbalance w coronary supply of blood and myocardial demand for oxygen and nutrients 

risk factors for Cardiac artery disease (CAD)

\-age, family history, male, female after menopause

\-smoking, hypertension, diabetes and insulin resistance, high cholesterol (dyslipidemia), obesity, sedentary lifestyle (sitting a lot)

cardiac angina (stable)

\-reversible chest pain caused by myocardial ischemia

\-from increased myocardial oxygen demand (exercise or emotional stress)

 -rest allows for return of adequate perfusion and symptoms disappear

cardiac angina (unstable)

\-acute coronary syndrome (medical emergency)

\-reversible myocardial ischemia, warning for myocardial infarction

\-new onset angina, angina that occurs during rest or doesn’t resolve, increase in frequency or severity 

myocardial infarction (heart attack)

\-acute coronary syndrome (medical emergency)

\-prolonged ischemia leads to irreversible death of cardiac muscle 

\-STEMI and NSTEMI and elevated levels of troponin and CK-MB

venous stenosis

\-valve orifice is constricted and narrowed 

 -aortic stenosis

-age calcification of aortic valve, congenital bicuspid valve, or inflammation from rheumatic heart disease

-aortic semilunar valve narrows causing loss of blood flow from left ventricle into aorta

             -causes left ventricle to become enlarged or hypertrophic which increases cardiac O2 demand 

valvular regurgitation

\-valve fails to shut completely, can also be called valvular insufficiency or incompetence 

\-aortic regurgitation 

-from congenital bicuspid valve, chronic hypertension, rheumatic heart disease, connective tissue disorders (ankylosing spondylitis)

-aortic valve leaflets don’t close properly during ventricular diastole which leads to a backwards leak of blood flow from aorta to left ventricle  

             -left ventricle compensates by becoming enlarged or hyperthrophic that leads to an increase in cardiac oxygen demand 

left sided heart failure (congestive heart failure)

\-systolic heart failure (HFrEF) or diastolic heart failure (HFpEF), or both

\-systolic heart failure also known as heart failure with reduced ejection fraction of

right sided heart failure

\-right ventricle cannot give enough blood flow into the pulmonary circulation while maintaining a normal venous pressure

-can be caused by pulmonary hypertension or from severe left heart failure bc there’s an increase in pressure filling in the left ventricle that then gets retracted back into the pulmonary circulation

-when the pressure retracts back the heart has to do more work which causes right ventricular hypertrophy 

\-symptoms include systolic and diastolic failure. Increase in presuure also causes edema, hepatosplenomegaly, and jugular venous 

Tetralogy of Fallot

\-might be life threatening congenital disorder. 

                        -4 main heart defects

                                    1) large ventral septal defect (VSD)

                                    2) overriding aorta over the VSD

                                    3) Pulmonary stenosis

                                    4) Right ventricular hypertrophy

clinical manifestations of tetralogy of fallot

\-tet spells (hyporcyanotic spells)

          -triggered by crying or exertion 

patent ductus arterioles

\-Ductus arteriosus do not close 

          -normally occurs within a few hours of birth

  -will then lead to shunting of blood from aorta to pulmonary arteries

clinical manifestations of patent ductus arterioles

\-machinery like murmur, hypercyanotic spells, signs of pulmonary over circulation, weak pulses

cough

protective reflex to help clear airway w explosive expiration

sputum

mucus that is coughed up, can be examined to aid w diagnosis

hemoptysis

coughing up blood

kussmaul respirations

\-deep rapid breathing pattern seen in patients w metabolic acidosis -compensation for metabolic acidosis 

cheyne stoke respirations

\-alternating periods of deep and. shallow breathing and apnea 

\-brain injury (cortex is gone) 

hypoxia

\-reduced oxygenation of cells in TISSUE (monitor on finger)

hypoxemia

\-reduced levels of arterial oxygen (BLOOD), (reduced PaO2- ABG)

ARDS

\-most severe form of acute lung injury 

\-caused by acute inflammation and alveolocapillary injury 

-bilateral lung infiltrates on x ray, increase delivery of O2, patient levels are still low in blood (hypoxemia)

clinical manifestations for ARDS

\-dyspnea and hypoxemia w poor response to O2 supp

 -hyperventilation and respiratory alkalosis (removes CO2)

 -decreased tissue perfusion, metabolic acidosis, organ dysfunction

 -increased work of breathing and hypoventilation

 -hypercapnia, resp acidosis, worsening hypoxemia 

 -__decreased cardiac output, hypotension, death__ 

pneumonia

\-infection of lower respiratory tract

\-caused by bacteria, viruses or fungi

\-community acquired (CAP), hospital acquired (HAP), ventilatory associated (VAP)

clinical manifestations of pneumonia

\-viral upper respiratory tract infection leads to viral or bacterial pneumonia

 -cough, pleuritic chest pain, fever, chills, malaise

  -if severe, maybe sepsis 

asthma

\-chronic inflammatory disorder of bronchial mucosa 

\-causes bronchial hyperresponsiveness and airway constriction

 -is reversible 

               -constricted bronchi can return to normal and stop impeding airflow

early asthmatic response

\-dendritic cells present antigen to helper T cells, releases inflammatory cytokines/chemokines that trigger bronchospasm and lead to airway obstruction

\-peaks within 30 min of exposure to antigen, resolves within 1-3 hours

late asthmatic response

\-release of chemokines during early response and results in gathering of other WBCs which leads to inflammation and injury to pulmonary tissue if not treated

\-begins 4-8 hours after early response and results in bronchial hyperresponsiveness (increased sensitivity to antigens)

clinical manifestations for asthma

\-asymptomatic between attacks

\-first symptoms include chest tightness, dyspnea, wheezing, coughing, tachypnea, tachycardia

\-severe, respiratory distress, respiratory acidosis, acute respiratory failure 

\-ominous signs: absent breath sounds of chest auscultation

\-status asthmaticus: life threatening where bronchospasm is not reversible by typical treatment methods

COPD

\-risk factors: smoking, occupational, air pollution, genetic factors

\-not fully reversible 

emphysema (alveoli inflammation)- pink pitcher

\-inhalation of irritants leads to inflammation of alveoli 

\-destruction of alveoli via breakdown of elastin in septa and permanent enlargement of gas exchange airways

chronic bronchitis (goblet cell inflammation)- blue bloater

\-inhalation of irritants leads to inflammation of bronchi goblet cells

\-stimulates mucus secretion that becomes thick and impairs bronchial ciliary function

pulmonary embolism

\-blockage of part of the pulmonary vascular bed from a thrombus, embolus, tissue fragment, lipid, foreign body, amniotic fluid, or air bubble 

                 -most likely in a deep vein in the thigh/calf (DVTs)

risk factors for pulmonary embolism

\-venous triad: venous stasis, hypercoagulability, injury to endothelia cells that line vessel

clinical manifestations for pulmonary embolism

\-sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia, anxiety, cardiac arrest and death

 -doesn’t appear on regular CT or x ray so need a CT ANGIOGRAM

croup

\-laryngotracheobronchitis

\-infection of the upper airway that leads to obstruction

 -caused by viral infections, cant do anything for it so it needs to go away on its own

 -common in ages 6 months to 5 years

clinical manifestations for croup

\-seal like cough, hoarse voice, inspiratpry stridor, (inflamed larynx)

 -may need hospitalization if happens when sleeping or at rest 

cystic fibrosis

\-autosomal recessive genetic disorder leading to multisystem organ disease

 -gene mutation leads to abnormal chloride channel

-cells are unable to transport chloride outside of the cell, so it doesn’t attract water to help moisturize and thin secretory mucus

-instead, cells produce a dehydrated, thickened mucus which is prone to sticking together

-injurious and can cause obstruct bronchioles, chronic inflammation, increase risk of infection

clinical manifestations for cystic fibrosis

\-severe pneumonia, persistent cough or wheeze, excessive sputum production, hemoptysis, chronic hypoxia (nail clubbing)

Risk factors for Sudden infant death syndrome

\-first 2-4 months of life, during nighttime sleep, winter months

\-preterm or low birth weight, multiple births, positive family history, environmental stressors 

Prevention strategies for sudden infant death syndrome

\-avoid prone sleeping (on belly or side)

\-avoid soft bedding, toys and blankets in crib

 -avoid bed sharing

 -encourage breast feeding and routine immunization

determinants for obstructive uropathy

\-cause of the lesion, duration of blockage, location of blockage, degree of completeness, and whether it involves one or both urinary tract systems

kidney stones

\-upper tract obstruction

\-masses of crystals, proteins, or mmineral salts form in urinary tract

\-supersaturation of one or more salts leads to precipitation and then crystallization of aggregation into stone

inhibitors of kidney stones

\-pyrophosphate, potassium citrate, magnesium

clinical manifestations of kidney stones

\-renal pain, very painful along back, signs of urinary obstruction 

cystitis (UTI)

\-inflammation/Infection of bladder

\-caused by genitourinary bacteria flora overgrowth or travel backward into host body (retrograde) 

\-at risk: women, on antibiotics, catheters, diabetes mellitus, dysuria, hematuria, cloudy foul smelling urine, flank pain

pyelonephritis

\-infection of kidney

\-risk factors

-female, kidney stones, vesicoureteral reflux, pregnancy, neurogenic bladder, instrumentation, sexual trauma

 -clinical manifestations

-acute onset of systemic symptoms (fever and chills), costovertebral angle tenderness, UTI symptoms

                                  

acute kidney injury

\-decreased GFR, increased serum creatinine, increased blood urea nitrogen (BUN), and reduced urine output

pre renal acute kidney injury

\-occuring in the body

\-not enough renal perfusion leads to decrease in glomerular filtration pressure

-hypotension, hypovolemia from blood loss or hemorrhage, renal vasoconstriction from NSAIDS (ibuprofen)

infrarenal acute kidney injury

\-something wrong with kidney cells

\-direct injury of renal parenchyma or interstitial cells           

-acute tubular necrosis, exposure to nephrotoxic contrast dye, acute glomerulonephritis, graft rejection

post renal acute kidney injury

\-urinary tract obstruction leads to increase intratubular pressure and decreased GFR

            -tumors, kidney stones, neurogenic bladder

chronic kidney disease

\-progressive loss of renal function, most likely caused by underlying systemic diseases such as uncontrolled hypertension, diabetes, systemic, lupus erythematous or intrinsic kidney disease 

\-clinically measured by decreased GFR, increased serum creatinine, increased blood urea nitrogen (BUN), degree of albuminuria, and reduced urine output

proteinuria and angiotensin II

\-proteinuria is involved in tubulointerstial injury by promoting inflammation and progressive fibrosis 

\-angiotensin II promotes glomeruli hypertension that can progress into tubulointerstitial fibrosis and scarring

clinical manifestations of chronic kidney disease

\-symptoms don’t appear until after 25% of renal function is lost 

 -may develop life-threatening hyperuremic syndrome 

-toxic build up of end products of metabolism leading to hypertension, anorexia, nausea/vomiting, diarrhea, constipation, malnutrition, weight loss, seizures, cardiovascular disease 

hypospadias

\-urethral opening on the ventral side or under surface of the penis 

hemolytic uremic syndrome

\-hemolytic anemia, thrombocytopenia, and renal impairment

\-common community acquired cause of Acute renal failure in children 

clinical manifestations of hemolytic uremic syndrome

\-associated w bacterial and viral endotoxin agents (E coli)

                       -bacterial toxin lysis RBCS and activated coagulation cascade and platelets. The toxin then travels to the kidney and lysis endothelial basement membrane cells of glomeruli. Glomeruli arterioles swell and fill w fibrin clots. RBCs are further destroyed when they pass through swollen glomeruli blood vessels 

hematemesis

bloody vomit

hematochezia

bright red bloody stool

melena

dark black and tarry stools (digested blood)

occult bleeding

not visible to naked eye, microscope

Gastroesophageal reflux disease (GERD)

\-acid and pepsin reflux from the stomach into the esphagus which causes esophagitis

\-abdominal pressure can contribute to gerd

-causes vomiting, coughing, lifting, bending, obesity, pregnancy,

clinical manifestations for GERD

heart burn, chronic cough, laryngitis, asthma attacks, sinusitis, upper abdominal pain within 1 hour of eating

peptic ulcer disease

break in mucosal lining of lower esophagus, stomach, or duodenum (common)

\-superficial (erosion) or deep

\-risk factors

* H pylori infection, NSAIDS usage, alcohol or smoke use, obesity, COPD, cirrhosis, old, chronic stress (inflammation)

clinical manifestations of gastric ulcer

\-epigastric pain that gets worse 30 min to 2 hours after eating when empty stomach and is relieved by food and antacids

clinical manifestations of gastric ulcer

\-common to experience pain right after eating

ulcerative colitis

\-IBD

* chronic inflammatory bowel disease that causes ulceration of colonic mucosa
* limited to COLON only, affects sigmoid colon and rectum
* lesions only in mucosa

ulcerative colitis clinical manifestations

large volume or bloody diarrhea w abdominal cramping pain and increased urge to defecate

chrohns disease

chronic inflammatory bowel disease that causes lesion in any part of digestive tract (from mouth to anus)

\-skip and deep lesions

chrohns disease clinical manifestations

\-diarrhea that may or may not be bloody

\-anemia, weight loss, nutritional deficiencies (b12, folic acid, and vitamin D)

portal hypertension

\-high blood pressure in the portal venous system by resistance to portal blood flow

\-common cause is liver cirrhosis that leads to portal vein fibrosis and obstruction

\-complications

* -varices in stomach, rectum, abdominal wall, spleen, esophageal. rupture of these is life threatening
* splenomegaly, hepatopulmonary syndrome

cirrhosis

inflammatory fibrotic disease that disrupts liver function and structure. normally irreversible

\-caused by:

* alcohol abuse, hepatitis C, fatty liver disease and fatty liver steatohepatitis, binary cirrhosis (from bile duct obstruction)

\-hepatic formation of nodular and fibrotic tissue decreased liver function

\-biliary channels become obstructed and cause portal hypertension

\-hypertension causes blood to be shunted away form the liver and causes hypoxic necrosis to develop

ascites

overload of fluid in the peritoneal cavity from portal hypertension

hepatic encephalopathy

\-impaired behavioral, cognition, and motor function

\-from build up of toxic end products like ammonia (interstitial protein digestion and produced by intestinal microflora)

* -ammonia converted into urea in liver and excreted in urine
* -when ammonia crosses threshold concentration, can then cross blood brain barrier
* intracranial ammonia convert to glutamine and becomes neurotoxic which may lead to hepatic encephalopathy then cerebral death

jaundice (icterus)

\-yellowish/greenish discoloration of skin from excess conjugated or unconjugated bilirubin

* biliverdin is a byproduct of heme that gets converted into unconjugated bilirubin in plasma
* unconjugated is conjugated in the liver and excreted through stool
* undone may excrete in urinecause

causes of excess bilirubin

\-extrahepatic(gallstones), intrahepatic (liver disease, cirrhosis or hepatitis), or prehepatic (excess hemolysis) 

acute pancreatitis

\-sudden onset acute inflammation of pancrease

 -caused by gallstones that block the bile or pancreatic ducts

clinical manifestations of acute pancreatitis

\-acute epigastric abdominal pain that becomes worse with eating

 -nausea and vomiting 

 -systemic inflammation signs (fever, elevated WBC)

cleft lip and cleft palate

\-embryonic developmental abnormality caused by gene environmental infractions

                        -risk factors

\-maternal vitamin B deficiency (B6, B12, folic acid)> cofactor for cell growth       

\-maternal smoking and alcohol use

\-maternal diabetes

                        -both can lead to feeding and swallowing difficulties 

                        -treatment

                                    -surgical correction at 3-6 months

primary amenorrhea

\-primary (kid)

                        -failure to develop menses and secondary sex characteristics by 13

\-failure to develop menses by 15 not including secondary sex characteristics

primary amenorrhea \*compartment I:

\-anatomic defects of the outflow tract (normal ovaries but not vagina or uterus)

primary amenorrhea \*compartment II:

\-ovarian disorders (gonadal dysregulation)

primary amenorrhea \*compartment III:

\-disorders of anterior pituitary gland (pituitary dysregulation, tumor, traumatic brain injury)

primary amenorrhea \*compartment IV:

\-disorder of CNS or hypothalamic factors

               -tumor, stress, anorexia, infection, traumatic brain injury

Secondary amenorrhea

\-previous menstruation however absence of regular menses for 3 months or irregular menses for 6 months

\-most common cause: 

\-unknown pregnancy, thyroid dysfunction, stress, exercise, low body weight, hysterectomy (tubes tied), asherman syndrome