patho things i dont know

iatrogenic

ex. infection from a foley cath

incidence

rate at which new cases occur over a set time

prevalence

total number of disease cases at a certain time new and old

hypertension imposes extra workload on the left ventricle, causing this. symptoms are SOB, chest pain, syncope, irregular heartbeat

CH

this condition is a result of hyperplasia and it alters glucose levels so they often test for it with glucose tolerance

acromegaly

chemical

vascular response involves what mediators

tissue injury vascular response

cell derived

what kind of mediators are WBC, platelets, endothelial or damaged tissue cells

plasma derived

what kind of mediators are complement system, kinin system, and clotting system

acute inflammation vs chronic (cells involved)

acute= PMNs, platelets, mast cells, neutrophils.

Chronic= macrophages, lymphocytes, monocytes, fibroblasts

ask which are phagocytes

sinusitis

cant get mucous out bc of inflammation of sinuses

primary cause is viral infections

acute is 4-8 weeks, chronic is treated with steroids as well as antibiotics

tissue healing and repair

vitamins needed for every phase of wound repair

a and c

primary intention and secondary intention healing

primary is cleaner and smaller and stuff, secondary is opened and slow and heals from bottom up

RA (3 labs, CMs, patho)

-elevated ESR and CRP, presence of RF

-basically arthritis but tired, symmetrical, exacerbations, nodes, pannus

-autoimmune attack on joints

acute gastritis causes

long term NSAID use,

H. Pylori

extreme stress

alcohol, caffeine, smoking

(use PPIs and antacids)

chronic gastritis can cause what

impaired absorption of B12, impaired production of gastric acid, anemia

crohns unique sign and patho, common location,

skip lesions, chronic inflammation (granulomatous- thick) in the small intestine

obstructions can result

ulcerative colitis patho and location

chronic inflammation mostly superficial in colon, can cause more bleeding issues and anemia

what is the 3rd line of defense against infection

immune system

most common opportunistic infection and its deets

oral thrush

maceration and fungal infection

function of antimicrobial, antibacterial, antifungal drugs

antimicrobial: destroy and alter cell structure of pathogens

antibacterial: inhibits synthesis of cell wall

antifungal: binds to cell membrane to increase permeability

viral hepatitis specific signs, treatment

-jaundice, dark urine, clay stool

-antivirals, low fat diet

walled off area of bacteria (granuloma) in TB is called

ghon focus

pyelonephritis patho, most common cause, manifestation triad

infection/inflammation of renal parenchyma causes scarring

-urinary obstruction like kidney stones, E. Coli

-fever, cva pain, N/V

what type of meningitis is less severe and often resolves without treatment, specific CMs

viral

photophobia, nuchal rigidity, kernigs and brudzinskis (with neck) signs

along with systemic, what organ will be affected by malaria

liver

difference between t lymphocytes and b lymphocytes, NKC

T: from thymus, 3 types (cytotoxic, helper, suppressor)

B: from bone marrow, become plasma cells and antibody producers

NKC: natural killer cells, primary defense, innate

difference between IgG and IgE

IgG: most common, active against a lot of toxins, viruses and stuff and activates complement

IgG: stuck to mast cells, stimulates histamine for allergic reactions

central vs. peripheral organs

C: bone marrow, thymus

P: spleen, lymph nodes and lymph tissue

innate vs adaptive immunity

types of hypersensitivity reactions 1, 2 and 3

1: mast cells and IgE release through blood (anaphylaxis)

2: specific organs (rh isoimmunization)

3: whole body (lupus)

aids patho and stages

uses rna transcription to change genetic makeup of cells, loss of immunity due to loss of CD4 T lymphocytes

causes you to get more rare diseases.

kaposi sarcoma (cancer that comes from herpes virus)

0- positive infection

1- over 500 cells

2- 200 to 499 cells

3- under 200 cells

anaphylaxis CMs

bronchospasm, itching, angioedema, BP drop

SLE symptoms

-butterfly rash, joint pain/swelling, fatigue, swelling around heart and lungs, proteinuria, ulcers, arthritis

explain rh isoimmunization

normally blood between mom and baby dont mix, but when someone has an amnio, miscarriage, ectopic, or abortion the blood can mix, and if they are different rh types, the mom will make antibodies against the babys blood. If this occurs, blood mixing in the NEXT pregnancy will cause a type 2 hypersensitivity reaction and attack the baby, resulting in hemolytic disease.

then the baby can have hearing loss, learning problems, cerebral palsy, elevated bilirubin

treat with rh immunoglobulin

fluid compartments

intracellular and extracellular (interstitial vs intravascular)

hypervolemia

increase in extracellular volume from:

-increased sodium, aldosterone

-decreased intravascular fluid, albumin

can result in:

-symptoms, Decrease in hematocrit, serum osmolality, serum sodium, BUN, BNP

hypovolemia

-from VPPS losses, hyperventilation, hemorrhage, third spacing

-Decreased skin turgor, ortho and postural bp, urine output, perfusion

-increase in hematocrit, BUN, spec grav, osmolality, sodium, ADH, SERUM POTASSIUM AND SODIUM

Hyponatremic dehydration: sodium, type of fluid loss, fluid shift

Low sodium, hypertonic loss, fluid shifts into the cells (causing low bp)

isonatremic dehydration: sodium, type of fluid loss, fluid shift

(most common) normal sodium, isotonic fluid loss, no fluid shifts

hypernatremic dehydration: sodium, type of fluid loss, fluid shift

high sodium, hypotonic fluid loss, fluid goes from in the cell to outside the cell because its so salty out there, causing cellular dehydration

hypotonic iv fluids cause

water to move from extra to intracellular space

hypertonic iv fluids cause

water to move from intra to extracellular space

types of cirrhosis (scarred liver)

alcoholic, biliary, post-necrotic

albumin- made by liver, makes sure fluids doesnt leak from vessels and tissue

-decreased production of clotting factors, coagulation disorders

-palmar erythema, spider angioma, peripheral edema, ascites, flapping tremors, toxic ammonia levels, varices

hypokalemia

normal pH, bicarb, PaCO2

7.35-7.45

22-26

35-45

anion gap=

sodium — (chloride and bicarb),, big gap= acidosis

ways of regulating pH

lungs: control elimination of CO2

Kidneys: excrete H+, reabsorbs and generates new bicarb

(chemical) bicarb buffer system: most important—> weak acids or bases exchange for strong ones to neutralize

(chemical) KH exchange: excess H+ is exchange for K+ across the membrane

(chemical) Protein buffer: largest—> intracellular proteins, albumin, and plasma globulins combine with or liberate H+ (amphoteric)

repiratory: chemoreceptors detect changes in PaCO2 and pH—> increased ventilation decreases PaCO2 and H+ to prevent acidosis

how to determine the acid base imbalance

respiratory involves weird CO2 level (up= acidosis)

metabolic involves weird bicarb level (up= alkalosis)

acid-base imbalance causes

metabolic acidosis: overdoses, liver failure, hyperkalemia, hyperchloremia, diarrhea, kidney injury

metabolic alkalosis: vomiting, diuretics, hypokalemia, hypocalcemia, hypochloremia, hypomagnesemia, antacid abuse, inadequate renal perfusion

respiratory acidosis: hypoventilation, over-sedation, brain stem dysfunction, OSA, acute resp distress, COPD, pneumothorax

respiratory alkalosis: hyperventilation, anxiety/pain, respiratory distress, stroke/head injury

types of chemoreceptors for ventilation

peripheral: in the aorta and carotid, detect oxygen levels, respond to low levels by increasing ventilation

central: in the brain, levels of PaCO2

V/Q mismatch

either the lungs are ventilated but not perfused or the lung is perfused but not ventilated

(ex. PE and atelectasis)

hypoxemia and hypoxia

decreased oxygen leading to decrease in partial pressure of oxygen, leads to hypoxia

hypoxia first sign is restlessness/anxiety

cancer patho

neoplasms: irreversible deviant cell clusters that have autonomy and anaplasia

cancer: highly invasive and destructive neoplasms

—caused by alteration in genes that control cell repro, growth, differentiation and death (acquired mutations are most common but also can be genetic)

mutator genes: repair DNA, protect genome

protooncogenes: normal genes

oncogenes: mutated protooncogenes that cause cells to divide and multiply like crazy

tumor suppressor genes: regulates cell division and death rate

initiation promotion progression theory

initiation: causes mutation in cell

promotion: oncogenes activated, dependent on exposure to promoter

progression: independent growth, no longer need the promoter

leukemia acute vs chronic and patho VERSUS lymphoma

rapid production of abnormal WBCs, philadelphia chromosome for CML

versus

lymph tissue tumors, abnormal B and T cells (hodgkin— neck lymph nodes, night sweats, REED-STERNBERG CELLS or non-hodgkin— systemic)

synovial membrane has ______ blood supply, tendons and ligaments do NOT

rich

fat embolism

can be from a fracture, first symptoms include subtle change in behavior, then non-blanching petechial rash

types of bone cancers

osteosarcoma, ewing sarcoma, chondrosarcoma

osteoarthritis

-progressive loss of articular cartilage

-synovitis

-bone spurs

kidney functions and RAAS

filters blood, F/E balance, produces vitamin D and erythropoietin and renin (for bp)

GFR: how fast the glomerulus is filtering blood

polycystic kidney disease

genetic autosomal dominant, replacement of kidney tissue with cysts, earliest CM is HYPERTENSION, high risk of fluid volume overload

what is in white and gray matter

white= axons and dendrites, myelin

gray= cell bodies outside in the brain

PNS components

somatic (cranial nerves, spinal nerves, peripheral nerves)

autonomic (sympathetic and parasympathetic)

pyramidal vs extrapryamidal

extra= basal ganglia, background and suportive movement like coordination and balance

pyramid= delicate movement

parkinsons

tremor, rigidity, bradykinesia

progressive destruction of nigrostriatal pathway, reduction in dopamine

MS

demyelinating autoimmune disease of CNS

plaques in brain, spinal cord, optic nerve

VISUAL FIELDS is first sign

steroids for exacerbations

cerebral palsy

lack of oxygen event during fetus-ery damaging upper motor neurons, not progressive

spastic, dyskinetic, ataxic, and all the plegias

seizure precautions

increased ICP

increased BP, lower HR, papilledema

negative vs positive feedback loop

hormones in stress response

corticotropin releasing hormone, acth, cortisol, catecholamines

GAS

alarm stage triggers HPA axis, sympathetic ns and body defenses

resistance begins w actions of adrenal hormones, mobilization

exhaustion only happens when stress doesnt go away after adaptation

too little hormone

DI: too little ADH, diuresis increasis, water intoxication and dehydration

-treat w hydration and desmopressin

Hypothyroidism: complication is myxedema coma

Addisons: autoimmune destruction of adrenal cortex, acth increases to help, causing farmer tan adn like skinny weak sick dehydrated ppl. hyponatremia, hyperkalemia

-fluid replacement and steroids, increase sodium

too much hormone

SIADH: too much ADH commonly from tumor, water accumulates in cells and sodium is diluted in extracellular space, causing hypotonic hyponatremia, NOT PEE ENOUGH

-treat w iso/hyper IV, diuretics

Hyperthyroidism: graves disease is autoimmune, binds to tsh receptors. goiter, crazy thin and oily and eyes poppin

—treat by just taking that bitch out w surgery or iodine

Cushing: excess glucocorticoids from adrenal cortex from long term steroid use or tumors. fat trunk, back and head with glucose intolerance. test cortisol levels in urine

-remove the bad shi

hormonal disease effects chart

NORMAL age related changes

longer healing, less padding and temp control, more inactive sweat glands, dry skin

decrease in muscle and increase in fat, causing decrease in total body water and F/E effects

immune senescence, enhanced autoimmune stuff, reduced allergy response, decreased Tcell function and Bcells dont make antibodies as fast, cancer not detected as quickly

decrease in brain mass, neurons, synapses, and myelin. bigger ventricles and altered neurotransmitter production, slower reaction times, decreased blood flow to brain

presbyopia and presbycusis

loss of bone, more brittle bones, joint cushion worn down, synovial fluid gets thicker, sarcopenia, mild kyphosis

less springy lungs, alveolar enlargement

decreased resting HR, heart valves thicken and harden, increased workload on left ventricle

declining ingestion/absorption and movement in gi tract, liver function declines, reduced renal blood flow

less elastic baldder and urinary retention, stress incontinence, prostate issues

even though more common in older adults, still ABNORMAL changes

cataracts, glaucoma, MD, parkinsons, hyperkyphosis, constipation, full incontinence

older adult assessment tools

MOCA, SPICES, morse fall risk, TUG, SCALES (malnutrition)

progeria

autosomal dominant, hyaluronic acid in blood

alzheimers

amyloid plaques, tau tangles, neuronal loss

1: minimal cognitive impairment

2: mild, evident only to self

3: mild, evident among family, friends

4: moderate, evident by examiner

5: moderately severe, requires assistance for day to day activities

6: severe, significant personality changes, assistance with ADLs, episodes of incontinence, delusions and wandering

7: very severe: loss of ability to respond to environment

malnutritions

marasmus: starvation, skinny

Kwashiorkor: protein deprivation with adequate CHO intake, big round belly

protein contains nitrogen, need to maintain nitrogen balance for protein synthesis and production of things like hormones, neurotransmitters, cell mediators, antioxidants

macro vs micronutrients

macro: protein (10% to 35%), carbs (45% to 65%), lipids (20% to 35%)

micro: vitamins (fat soluble ADEK, water soluble BC) and minerals

water

nitrogen balance

homeostasis is zero nitrogen balance

positive is when the intake exceeds the output and can happen in growth periods, tissue repair, hypothyroidism, pregnancy, and bodybuilding

negative is when output exceeds intake and can happen with prolonged immobility, malnutrition or absorption, burns, trauma, and surgery

carbs

monosaccharides (glucose and fructose), di-/oligosaccharides (sucrose and lactose) and polysaccharides (starches and fiber)

for energery, reducing cholesterol, fiber aids gastric motility

Vitamins

organic substances the body needs but isnt able to manufacture

aids in metabolism of macros, helps develop genetic materials and hormones and collagen and NS tissue

Vit K produced in the intestines, newborns get a Vit K shot because they arent getting it from solid food and it helps to clot blood and form bone

Vit D absorbs and metabolizes calcium and phosphorus

Vit C does iron absorption, metabolizes amino acids, synthesizes steroid hormones

Vit B metabolizes carbs, folate forms blood cells in the bone marrow

minerals

inorganic substances critical to cellular processes

sodium, potassium, calcium, phosphorus, magnesium, sulfur (macros)

iron, zinc, flouride, copper (micros)

they constitute bone, hemoglobin, enzymes, hormones and chemical mediators, they mediate impulses and maintain fluid and acid/base balance

appetite hormones from hypothalamus

when full, increased BG triggers the release of insulin, and increased lipids trigger adipose tissue to release leptin

when tummy is empty, we release ghrelin

obesity

hypertrophic: bigger adipose cells

hypercellular: more adispose cells (often starts in childhood)

adipocytes synthesize triglycerides (three fatty acids)

measure mid-arm circumference

iron deficient anemia

Cx: chronic hemorrhage, iron malabsorption, high iron demands, inadequate iron intake, milk and celiac (??)

insufficient iron stores to meet needs for RBC development

low RBC, hematocrit, and hemoglobin, stool guaiac positive (black and tarry), PICA

microcytic (smaller RBCs) and hypochromic (less vibrant red)

celiac

T-Cell mediated hypersensitivity reaction

gluten is found in wheat, rye, oats, barley

strong hereditary component

lab value for nitrogen use in the body

BUN- the nitrogen in your blood that comes from urea

proteins broken down in intestines produce ammonia

liver changes ammonia to urea

kidneys filter out urea from the blood

insulin increases when what increases?

glucose and potassium

altered perfusion: V/Q mismatch, impaired circulation, inadequate cardiac output, exccessive perfusion demands

V/Q mismatch: ratio is 0.8:0.9, resp disease and PE

impaired circulation: hemorrhage, obstruction or disruption in flow like atheroma or DVT, inadequate blood comp. or volume

inadequate cardiac output: inadequate blood comp or volume, impaired ventricular function (CHF or defect), structural defect (ASD and VSD), excess peripheral vascular resistance (aterial diseases), conduction defects (arrhythmias)

exccessive perfusion demands: prolonged exertion, metabolic disease (thyroidisms), increased work load

a rise in troponin means

u had a heart attack

a rise in what protein indicates inflammation

c-reactive

homocysteine

an amino acid from breakdown of animal protein that some of the B vitamins like folate break down. if theres a lot it can cause a heart attack or stroke

clotting stuff dont really need to know i think)

platelets

prothrombin time

partial thromboplastin time

international normalized ratio

central vs tissue perfusion

central: pacemakers, electrical cardioversion, ablation therapy, intraaortic balloon, cardiac valve surgery, cardiac transplant

tissue or local: bypass, graft, stent or angioplasty, endarterectomy (blade takes away buildup)

starlings law

if thangs were more stretched at the start there would be more output like balloon (contractility)

preload: more stretch, better flow (volume)

afterload: more resistance, less flow (constriction and dilation)

atherosclerosis process

monocytes adhere to the vessel wall and change configuration to macrophage i think?

then they eat up the LDL and become foam cells

group of foam cells is a fatty streak

calcification of the plaques is fibroatheroma

next step is MI or stroke

doesnt happen overnight