Patho Final - Old Content

Differentiate atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia.

Size or number

• Atrophy = size decrease

  • Due to decreased demand or supply

• Hypertrophy: increase in cell size

  • Increased demand

  • Skeletal and cardiac

• Hyperplasia: increase cell number

  • Increased demand

  • Skin, intestinal, gland, hepatic, reproductive (BPH)

Cell Type

• Metaplasia: From one normal cell to another

  • Chronic irritation/inflammation

  • New cell type is TOUGHER and better to survive in harsh condition

  • “Barrett’s esophagus”

  • Reversible

• Dysplasia: cells are MESSED UP

  • Chronic irritation or inflammation

  • New cell types are abnormal an do NOT function very well

  • Different than anaplasia (which is cancerous)

Using examples, interpret ABGs using the terms, metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis and compensatory mechanisms

• Metabolic Acidosis: Blood pH less 7.35

  • Too little BASE (HCO3) - ABG: Low HCO3/bicarbonate

    • GI loss of HCO3

  • TOO MUCH ACID

    • Renal failure

    • Ketoacidosis

  • Manifestations

    • Compensation: Kussmauls breathing - blow off CO2: LOW CO2

    • Disorient

    • Coma

    • Dysrhythmia

• Metabolic Alkalosis

  • ABG: HCO3 TOO HIGH

    • Loss gastric acids, bicarbonate ingestion, etc.

      • PH over 7.35

  • Manifest: Cardiac dysruthmia

  • Comp: Lungs attempt retain CO2 slowing RR, Kidney retain H+

    • ABG: High CO2

• Respiratory Acidosis:

  • CO2 TOO HIGH

  • Compensation: Kidney attempt reabsorb HCO3, Excrete H+

    • HCO3 ELEVATED, H+ LOW

• Respiratory alkalosis

  • BASIC

  • CO2 LOW

  • Comp: Kidney try reabsorb H+ and excrete HCO3

    • HCO3 LOW, H+ HIGH

Know how to solve problems look at exmapls// picture

Understand how transcellular shift regulates potassium ion and hydrogen ion concentration

• Potassium helps maintain intracellular osmolarity

• Controls cell resting potential

• Potassium-hydrogen transcellular shift (K+/H+)

  • Potassium exchanged for H+ to buffer changes in blood pH

• Acidosis

  • Reg intracellular potassium, high H+ inside bloodstream

  • Potassium from inside cells pulled into bloodstream, low potassium intracellular

• Alkalosis:

  • Reg intracellular potassium, low H+ inside bloodstream

  • Potassium moves from bloodstream into cells = high intracellular potassium

Describe how osmoreceptors and renin-angiotensin-aldosterone system (RAAS) maintain fluid balance.

Look at picture and STUDY

State the five cardinal signs of acute inflammation and describe the physiologic mechanisms involved in the production of these signs.

ALL THESE DUE TO THE VASCULAR STAGE (Local response)

• Local response is nonspecific, protective, coordinated

• Inflammatory mediators released at area

• Redness

  • Vasodilation to area causes redness, more blood

  • Vasodilation caused by inflammatory mediators (histamine and bradykinin) which enable blood vessels to dilate and become permeable

• Swelling

  • Vasodilation of arterioles is followed by enhanced capillary permeability

  • Fluid flows OUT of blood vessels into injured tissues = swelling

• Heat

  • Heat due to Increase blood

• Pain

• Loss of Function

Pain and loss of function caused by

• Chemical mediators, histamine, bradykinin, prostaglandin cause nerve endings to be senstiive

• Swelling causes pressure on nerve endings

• LOF

  • Pain and swelling limit/ restrict movement

  • Tissue damage or disruption can also

PAIN and LOF can come from chemical stage as well as vascular stage

• Chemical as a result of chemical mediators which can cause pain and disrupt tissues

Describe the processes of transcription and translation and identify the ultimate product

• Transcription:

  • Process of making RNA copy of DNA

    • Occurs in nucleus

  • Intiation RNA poly binds

  • Elongation

  • Termination

  • PRODUCT = mRNA (carry genetic code out of nucleus to ribosome)

• Translation

  • Happens at ribosome

  • mRNA provides code

  • tRNA provides amino acid

  • Ribosome forms peptide bonds

    • Intiation

    • Elongation

    • Termination

• PRODUCT = POLYPEPTIDE (protein)

Describe the etiology, pathophysiology and manifestations of atherosclerosis

• Causes/Etiology

  • Hypertension

  • Hypercholesterolemia

  • Smoking

  • Uncontrolled diabetes melitius

    • WHY? They all cause damage to endothelial tissue aka blood vessel tissue

• Steps:

  • Epithelial damge causes migration of WBCs (leukocytes) and platlets

    • These adhere to the endothelial tissue

    • Endothelial tissue becomes permeable

  • Macrophages are adhere to endothelial tissue (they were leukocytes, macrophages ARE specific type of leukocytes)

    • Start to engulf LDL

  • Foam cell formation

    • Macrophages migrate inside epithelial tissue and become foam cells (foam cells = lipid loaded macrophages, LIPIS = LDLs)

    • Smooth muscle begins to migrate upward to make a FIBROUS CAP

      • Underneath lies machrophages, foam cells, necrotic core, lymphocytes collagen

    • Adherence and entry of leukocytes

    • Adherence and aggregation of platlets

  • This is a atherosclerotic plaque now, causes FATTY STREAKS

    • If ruptures, causes major clotting to occur and

    • If NOT just ISCHEMIA

• Manifestations

  • Most common in:

    • Abdominal aorta + iliac

    • Coronary

    • Femoral, popliteal

    • Internal carotid

    • Verebral, basillar

  • Manifestations of

    • Stable angina

    • Dyspnea

    • Fatigue

  • If rutpure:

    • Mycardial infarciton

    • Unstabel angina

    • Cardiac death

    • Stroke

Define peripheral arterial diseases and explain S/Sx (including claudication, oxygen
demand/supply).

• PAD also known as Peripheral arterial occlusive disease

  • Atherosclerotic plaque obstructs blood flow to a LOWER extremity (peripheral)

• Risk factors:

  • Age, HTN, DM, SMoking

  • High fat diet, sedentary

  • Family history

• Flow chart:

  • Occlusion of arterial blood flow

  • Reduction in blood flow

  • Oxygen supply LOWER THAN Demand

  • Ischemia, aerobic metabolism

  • Pain (intermittent claudication - bc its in legs)

    • Pallor

    • Weak pulse

    • paresthesia - numbness tingling in lower extremities DUH

Describe hallmarks of stable angina

• Chest pain

  • Occurs when there is INCREASED myocardial oxygen demand (physical work, emotianl stress

• Relieved by:

  • Rest DUH

  • NItroglycerin

• From a FIXED ATHEROSCLEROTIC PLAQUE causing ischemia

• Very common - intial presentaiton for MANY people with coronary artery disease

So hallmarks = chest pain or pain, relieved by rest or nitro and caused by something

• Unstable is PAIN AT REST, and rest does not help duh

Explain how heart failure changes the following hemodynamic measurements: CVP, CO, pulmonary capillary pressure, and BP

• Systolic Heart failure: Heart does not PUMP ENOUGH OUT (due to weak ventricle)

• Diastolic: NOT ENOUGH BLOOD IN (due to stiff ventricle)

  • Dec CO

  • Dec SV

  • Decreaes BP as well, BP = CO x PVR

  • Also INCREASE pulmonary capillary pressure

    • Not enough out means BACKUP somewhere

• Backward effect

  • backup of blood into atriums and pulmonary vessels

  • LVF = pulmonary edema = cough, orthopnea, noctural sypnea

    • RVF - lower extremity edema

• Forward effect

  • Not enough out = dec BP

  • Dec BP = RAAS< ADH, SNS

    • Increase fluid retetnion = weight gain

Differentiate the three main categories and mechanisms of anemia (blood loss, hemolytic and impaired RBC production

• Blood loss

  • Acute vs Chronic

    • Acute = rapid blood loss from trauma, childbrith, vessel rupture, etc.

    • Labs = Normochromic Normocytic (BC its SUDDEN)

  • Chronic

    • Slow blood loss = GI Bleed or something

    • Leads to LOW IRON = iron deficiency anemia

    • Microcytic Hypochromic

• Hemolytic/ SICKLE CELL

  • Autosomal recessive disease

  • Mutation causes sickle cell anemia RBCS

    • Upon exposure to hypoxia or stress, RBC contorts into a sickle shaped

    • = Cant pass through capillaries = hypoxia due to obstruction

    • ALSO leads to excessive RBC breakdown = jaundice

  • NORMOCYTIC NORMOCHORMIC (why?)

• Impaired RBC production

  • Decreased production of RBCs by bone marrow

  • Essential nutrients

    • Iron: hemoglobin synthesis

    • Vitamin B12 and folic acid: for DNA and maturation

  • ANY Deficiency leads to decrease production leads to anemia

  • MICROCYTIC HYPOCHORMIC

    • Why- small due to lacking materials like hemoglobin

    • Hypochromic due to lacking hemoglobin

HEMOGLOBIN REQUIRES IRON

Describe how leukemias create each of these manifestations: anemia, thrombocytopenia, leukocytosis, neutropenia, bone pain, increased risk for infeciton

Leukemia general: Leukemia = a cancer of the blood forming tissues aka cancer of the bone marrow

Cancer of the bone marrow leads to overproduciton of abnormal white blood cells which CROWD OUT normal, healthy blood cells

• Anemia

  • Overproduction of abnormal/ immature white blood cells overcrowd the bone marrow and decrease RBC production/ growth

• Thrombocytopenia

  • Overproduction of abnormal/ immature white blood cells overcrowd the bone marrow and decrease RBC production/ growth

• Leukocytosis

  • Stem cell precursuros for T and B lymphocytes in bone marrow do NOT function and mature, leading to low WBC

  • Abnromal leukocytes = NOT DEVELOPED FULLY or NONFUCNTIONAL or UNCONTROLLED PROLIFERAITON

• Neutropenia

  • Bone marrow overcrowding

  • Fialure of normal cell formation, blasts stuck in early stages

  • Suppression by cytokines

• Bone pain

  • Due to overcrowding

• Increased infection risk

  • As a result of low WBC, neutrophils, etc. immune function is worsened

Create a table that compares and contrasts emphysema and chronic bronchitis in terms of most common cause- pathology and clinical manifestations.

Describe how COPD causes pulmonary hypertension (include hypoxic vasoconstriction in your explanation)

Chronic bronchitis - blue bloater

• CANT GET IN

• Mucus and edema inhibit ventalation = cough

• Chronic hypoxia + cyanosis

• Clubbing

• Chronic hypxoia = pulmonary arterial vasoconstriciton

  • Leads to RVF = JVD, ascited, ankle edema (BLOATER) hepatosplenamoagoly

• Chornic hypoxia leads to RIGHT SIDE HERAT FAILURE

Emphysema - PINK PUFFER

• CANT GET OUT

• Destruction of elastin = non recoil alveoli = CO2 retetnion

  • Chronic hypercapnia

  • Prolonged exhalation/ pursed lip

• BARREL CHEST, cant get out duh

• Diapghram pushed downard due to excess air

Explain changes in pulmonary function test (e.g., FVC, FEV1) in restrictive pulmonary diseases and explain what FVC and FEV1 are

• FVC = forced vital capacity

  • Total volume of air a person can FORECFULLY EXHALE after a full inhalation

  • Reflects LUNG VOLUME

• FEV1 = Forced expiratory volume 1 second

  • Volume of air exhaled in first second of FVC

  • Reflects airflow/ how QUICK air gets out

• Restrictive disease = REDUCED LUNG EXPANSION = total volume shrink

  • Pulmonary fibrosis

• Decreased FVC

  • If lungs CANT expand then there is less air to exhale and inhale

• FEV1 decrease

  • If total lung volume smaller, amount exhaled is smaller

  • FEV1 decreases propritonall to FVC

    • BC FEV1 is APART of FVC

FEV1/FEC ration

• If FEV1/FEC ratio over 0.9 its NO GOOD (aka closer to 1) THINK WHy

  • If its closer to one, that mean the amount dropped vs total amount out is very similar BECAUSE there is less to get out and its harder to get it out

    • After 1 sec its almost already all out

Describe the alterations in cardiovascular function that are characteristic of cor pulmonale.

Cor pulmonale = RIGHT SIDE HEART FIALURE

Cardiac alterations

• Right ventricular hypertrophy due to HIGH AFTERLOAD from pulmonary hypertension

• Rifht ventricular dilation THIS MORE IMRPOTANT (after time

• REDUCED CO

• Systemic venous congestion DUH

Signs and symptoms

• Chronic hypoxia

• Leads to a VQ mismatch

• Leads to pulmonary vasoconstriction

• Pulmonary hypertension

• RVH, RVF (increased workload)

• JVD, ascites, ankle edema

Describe the relationship between hypertension and the kidney dysfunction

Hypertension and kidney dysfunctino is BIDIRECTIONal

• If one gets wrose, the other gets worse

• AND VICE VERSA

• HTN caused by atherosclerosis or whatever

• Kidney disufnciton by dec GFR and urine output

  • WHY, decreased urine = increase fluid = more hypertension

  • More hypertention is wrose for kidney function, dec perfusion wahtever

Describe the three categories representing the causes of kidney dysfunction based on the mechanism of injury (prerenal, intrarenal, postrenal) and list examples of each dysfunction.

• Prerenal

  • Issue BEFORE kidney = REDUCTION OF RENAL BLOOD FLOW

  • Kidney not getting enough

    • Dec perfusion = dec GFR

    • RAAS activates = water + sodium retention

    • Concentrated urine

  • Examples:

    • Shock

    • Dehydration

    • Vasoconstriction

    • HTN

• Intrarenal

  • Problem WITHIN kidney itself = damage of tubules, glomeruli, interstria or vasculature

    • Kidney tissue is injured

      • Structural damage = impaired filtration, secretion, reabsorption

  • Acute Tubular Necrosis:

    • MOST COMMON

    • Ischemia, toxin, inflammation leads to sloughing of tubular endothelial cells which Block fluid flow through nephron

  • Acute interstitial nephritis

• Postrenal

  • Urine flow blocked = obstruction of

    • pressure backs up = hydronephrosis = decreased GFR

  • Example:

    • Stones, tumors, enlarged prostate (BPH)

Understand the pathophysiology and clinical presentation of chronic kidney disease

• Irreversible, progressive process with a GRADUAL onset

• CRF will progres to end stage renal failure

• Etiology;

  • Hypertension, Diabetes melitus, chornic glomerulonephritis

• Patho

  • Kidney damge leads to increasingly worse GFR

  • As neprhons fail, renal fialure issues set in

    • EPO

    • Vitamin D

    • Acid/base

    • Renin functions lost

• Signs and symtpoms

  • NO concentrated urine

  • Hyperphosphatemia - bone loss

  • Hypocalcemia - increase PTH

  • No EPO = anemia

  • Hyperkalmeia = acidosis

  • Metabolic acidosis

  • Fluid overload =

    • Edema

    • HTN

    • HF

    • Pulm edema

  • Neural

    • Ecephalopathy (cant filter)

    • Confusion, stupor

  • Thrombocytopenia

  • Anemia

Create a table that contrasts upper and lower motor neuron disorders (UMN and LMN) in terms of location of dysfunction and manifestations.

• UMN

  • Pathology in the CNS

    • Above brainstem = affects opposite side

    • Below brainstem = affect SAME side

  • Spastic/hypertonic paralysis

  • Hyperreflexia

    • (bc its affecting the root, think like disease affecting the generation = rapid fire)

• LMN

  • pathology in PNS

  • Affects SAME SIDE ALWAYS (bc the source of the problem is motor nerves that exit the spinal cord)

    • There is NEVER any crossover, lower left issue results in lower left issue

  • Flaccid/weakness paralysis

  • Hyporeflexia/ decreased reflexes

Briefly explain the mechanisms of ischemic stroke and state common causes

• Ischemic stroke = blocked blood flow to brain tissue

  • Tissue becomes ischemica = cerebral infarciton

• Common causes

  • Anyting that increases risk for developing atheroslcerosis = increased risk for ischemic stroke

    • It is cerebral atherosclerosis

    • Carotid stenosis

  • Atrial fibrialtion

• Ischemic penumbra = perimeter around CORE ischemic area

  • Rapid reperfusion of htis area is critical as it will also suffer infarciton soon after

    • HOWEVER, reprofusion causes free radicals to carry in blood stream (free radicals develop after cellular damage

Understand the mechanisms and S/Sx of Cushing’s triad

• Physiological response to elevated intracranial pressure

  • happens due to cerebral edema or anything else, bc skull CANT change shape/ give way

    • brain tissue damage = inflammation = edema in skull = increase ICP = cushing triad

• Parts:

  • Hypertension

  • Bradycardia

  • Irregular respirations

• Increaed ICP = reduced cerebral perfusion

  • Reduced cerebral perfusion leads to sympathetic activation

  • Leads to vasoconstriciton + hypertension (to help push blood into brain)

    • Leads to high pulse (widened pulse)

• Rise in BP = baroreceptor reflex = bradycardia

  • Bradycardia to compensate for high blood pressure

• Brainstem compression

  • Compression of pons and medulla leads to IRREGULAR RESPIRATIONS

Using the hypothalamic-pituitary-endocrine gland axis feedback mechanism, differentiate primary endocrine disorders from secondary endocrine disorders

• Hypothalamic-Pituitary-Hormonal axis

  • Hypothalamic portion of brain secretes RELEASING FACTOR (stimulates pituitary)

  • Pituarity secretes TROPIC/STIMULATING hormone (stimulates endocrine organ)

  • Endocrine organ secretes SPECIFIC HORMONE (to act on body)

• Primary = abnormality in peripheral gland

• Secondary = abnormality in pituitary

• Tertirary = abrnoamlity in hypothalamus

THINK NEGATIVE FEEDBACK LOOP

Look picture- SUPER EASY

Identify common signs/symptoms of Cushing’s Syndrome

• Cushing’s Syndrome = HYPERADRENALISM

  • Due to hyperactive adrenal gland which secretes too much cortisol

• Causes:

  • Endogenous cushings - tumor on adrenal gland or hyperplasia

  • Ectopic cushings - tumor release ACTH

  • Exogenous - long term or overuse of glucocorticoid

• S/sx:

  • Glucocorticoid excess

    • Hyperglycemic

    • Fat redistribution (buffalo hump and moon face, and large abdomen (increase waist to hip)

    • Thin skin + striae

    • Osteopororsis - due to increase bone resorption

    • Increase gluconeogensis = hyperglycemic DUH LOOK HERE

    • Decreased inflammation + immune response = more infection

    • Mood:

      • Irritible

      • Cognitive impariment

      • Fatigue (long term stress hormone = exhaustion)

  • Fluid, electorylte imbalance - Aldosterone/mineralcorticoid

    • Increase NA upkeep

    • Increase fluid

    • Increase BP

    • More acidic???

  • Androgens - Sex hormone

    • Females get hirsutism and menstrual irregularities

Recognize the chronic complications of diabetes including autonomic neuropathy, peripheral nephropathies, retinopathies, macrovascular complications, poor wound healing, foot ulcers, and infection

• Micro: AKA HYPERGLYCEMIC DAMAGE (affects smallest arterial blood vessels first) — RNN

  • Retinopathies (damage of eye)

    • Blindless

    • Cataracts

    • Glaucoma

  • Neuropathies (affects neurons (arterial vessels of neurons = small)

    • Sensory - pain sensation is blunted)

  • Nephropathy - very small

    • LEADING cause of chronic renal failure

• Macro:

  • Peripheral vascular disease

  • Coronary heart diease

  • Cerebrovascular disease

    • Stroke or TIA

Causes damage to larger epithelial tissue

Mos