Patho Exam 2

from written review pages

Anemia Definition + most common type

reduction of RBC mass

dec oxygen carrying capacity

Iron Regulation in the body

Location of Iron in the Body

Types of Iron Sources from Diet

Iron Absorption (+regulation)

4 main causes of Iron Deficient Anemia

RBC Measurements

Diagnostic Testing for Anemia

MCV

(low: fe def/microacidic anemia) (high: B12/folate deficiency)

Anemia Characteristics in Peripheral blood smear

small = low MCV

Bone Marrow Biopsy (anemia)

gold standard test, rarely needed, prussian blue stain limited stain bc little Fe in macrophages

Iron Studies Results comparing what factors appear at what stages of iron deficiency

ferratin, transferin, hemaglobin

(further along match further along steps)

Anemia of Chronic Disease: associated illnesses * (immune)

microbial: osteomyelitis, bacterial endocarditis, lung abscess, immune: R arthritis, regional enteritis, neoplasms: breast/lung, hodgkins lymphoma

Anemia of Chronic disease: associated illnesses

Anemia of Chronic Disease Etiology

IL-6 stip hepcidin → iron sequestration (attached to ferratin on mucosal lining, sloughed off)

Factors that influence Oxygen Economics (Supply vs Demand)

Ischemic Heart Disease (def, struct, funct)

structurally: CAD blcoked plumbing

functionally: reduce O2 carrying capacity: anemia or carboxyhemoglobin (ex from CO2 poisoning)

CAD (what it “is”)

blocked plumbing, leads to 90% of ischemic disease

blocked plumbing limit flow so can’t meet moments of higher demand

cause Angina Pectoris 3 presentations (before Ischemic Heart disease)

Angina Pectoris (def + discomfort location + necrosis?)

recurrent 15s - 3 min transient ischemic attacks

substernal/pericardial discomfort

no necrosis!

Types of Angina Pectoris (3 types)

Development of an AMI (acute myocardial infarc)

can occur without coronary atherosclerosis

AMI evolution under a microscope*

ami, i hear nothing from you for 4 hours then you tell me you have

coag necrosis, edema, hemorrhage

then on top of that you have both coag and contract nec plus pyknosis?

yeah neutrophils are here but you go on to tell me how now your breaking down and have no nuclei or nuclear striations then on top of that your myofibrils disintegrate

all for you to have granulation tissue, blood vessel, and collagen deposition

for you to inc collagen dep and dec cellularity

all to leave you with a dense collagenous scar?!

AMI Pathogenesis

Parts of a Neoplasia

parenchyma + stroma

Neoplasia Differentiation meaning

Tumor Grading System

Tumor Nomenclature

Benign vs Malignant Tumor

Tumor/Cancer Etiology (genetic types + aquired)

autosomal dom: “loss of funct mutation” cancer suppressor

autosomal recessive: issue with DNA repair

aquired: affect proliferation/regeneration (chronic gastritis/ulceraative coilitits)

7 Fundamental Changes in Tumors > malignancy

1) self-sufficient growth hormone (RAS- rat sarcoma gene)

2) uninhibited (lack P53 gene)

3) unlimited replicative potential (telomerase)

4) evade apoptosis (don’t sacrifice self)

5) sustained angiogenesis (no P53 to reg)

6) malignant capability

7) genomic instability (DNA mutations)

Carcinogenesis

Carcinogens

chemical: direct vs indirect

ionizing radiation

RNA: human T-cell lymphoma

DNA: human papillo + epstein barr

Pathogens (simple definition)

organisms that cause illness for their own survival “survival mode”

Human Microbiom % body comp

Opportunistic vs Primary/Obligate pathogens

TB, gonorrhea, T palladium, HIV

Pathogenicity

structural/biochemical mechanisms microbes use to cause disease

include invasiveness + toxicity

Pathogen Invasiveness + Toxicity

Portal of Entry (Pathogens)

parenteral routes = breaks in barriers

Virulence

pathogens ability to overcome host defenses and establish themselves

Colonization + Infection

colinization promoted by adherense mechanisms

Pathogen Adherence Specitivity (4 types)

Viruses (Basic Def)

usually can only use specific tissue/animal

What influences virus tropism? (3)

host receptors

environment

DNA transcription factors

Viral Mechanisms that Damage Host (3)

Viral Infection Presentation / Course of Infection

incubation 1-7, prodromal (hard hitting symptoms, mucus, contageous) 1-3 days, symptomatic 5-14 days (shed illness)

COVID 19 Viral entry / transmission

enveloped positive stranded RNA

spike S protein bind to ACE 2 receptors

COVID 19 Spread rates

COVID 19 Vaccines: Pfizer vs Johnson & Johnson

FVC vs FEV1

FEV1 / FVC ratio

Risk Factors for COPD

smoking (90% cases)

A1 Antitrypsin deficiency (inc susceptibility to effects of cigs)

resp infect + envi exposure

COPD (basic def)

chronic obstructive pulmonary disease

airflow limitation not fully reversible

Name the 3 concurrent factors that appear in COPD

chronic bronchitis of large airways, small airway disease (main site of resistance), emphysema (alveolar damage)

Net Effects of COPD (3)

1) airflow obstruction

2) lung hyperinflation “blue bloaters”

3) altered gas exchange

COPD: chronic bronchitis

Large airways, mucus, smooth cell hypertrophy, bronchial hyperreactivity (dec airflow)

COPD: small airway disease (elast)

bronchioles <2mm, major site of resistance, goblet cell replace surfactant cells, mononuclear phagocytes destroy elasticity, smooth muscle hypertrophy

COPD: emphysema*

irreversible alveolar damage without fibrosis

inflammation

neutrophil elastase ← → matrix metalloproteinases ECM

degrade inhibitor of eachother

detectable 9 yrs after last cig

Main Respiratory passages + what keeps them open (3)

trachea: cartilage rings, bronchi: cruved cartilage plates, bronchioles: pressure

Inspiration energy use / types of work

3-5% total energy

compliance (elastic), airway + tissue resistance

Inspiration vs Experation Mechanics

picture it expanding in all directions/shrinking in all directions

Asthma (basic def + phys changes)

chronic inflammatory disorder with reversible obstructive episodes

Physiological Changes in Asthma

goblet cells (mucus)

eosinophils/macrophage/mast cells > edema/inflam

smooth muscle hypertrophy

Asthma: symptoms

Asthma: triggers

Asthma: Airflow Resistance

usually airflow resistance at larger bronchioles near bronchi

alveoli / distal bronchioles not effected

during periods of disease state smaller bronchioles effected bc muscle constrict/mucous easier to effect

2 types of Asthmatic Responses

Atopic vs Non-Atopic

atopic: allergen, non-atopic: infection/inhaled pollutant

Asthma: Name 3 cytokines / their effects

T-cell activation + cytokines > inflam resp

IL-4 / 13 : blood based immune resp, IL-13 mucous too, IL-5 eosinophil allergic resp

Asthma: phases (2) early vs late

early phase: acute breathing / bronchiole obstruction (mucous, edema, muscle)

late phase: inflammation (epithelial cell chemokines recruit more mediators)

Asthma Attack

dyspnea/wheezing 1-several hours

caused by triggers (exercise, emotion, allergen, weather, viral infect)

aspirin

Asthma: Spirometry

assesses obstruction / reversability

Asthma: treatment

step plan according to symptoms

leukotriene Modifiers

IBS: systems that control GI system

enteric (intrinsic), autonomic (connect enteric to CNS) (symp/parasymp), CNS

IBS: GI reflexes (+ what they control)

short: enteric, long: ANS

control: secretions, peristalsis, segmentation

IBS (basic def)

chronic, continuous, or remittent

bowel disturbance + abdominal pain

Rome IV criteria

used to diagnose IBS

IBS: treatment (C vs D)

IBS: list the 5 components of IBS pathology

altered visceral (pain) perception, abnormal motility, abnormal secretion, triggers (bacterial growth), ANS dysfunction

IBS: altered visceral perception

[limbic system positive feedback loop]

spinal cord: central desensitization, serotonergic pathways

Limbic system: correlation with mood disorder + fear/sorrow inc pain, corticotropin > histamine > CRF positive feedback loop

aaaaaa spiders crawling up your back (afferent)

IBS: altered motility

small bowel dysmotility (transit times), colon dysmotility (varietion in slow wave freq, more common in IBS-D)

IBS: altered secretions (what cells do what)

secretory, goblet, crypt/pits lieberkuhn, tubular, complex glands

secretory: digestive enzymes, goblet: mucous, crypt/lieberkuhn: specialized secretory, tubular: acid/pepsinogen, complex glands: salivary/pancreatic

IBS: triggers

65-84% IBS pt have bacterial overgrowth of small intestine

post-gastroenteritis

food intolerances (lactose, sorbitol, fructose)

psychological

IBS: ANS dysfunction

main characteristic of IBS, C: inc sympathetic + vagal tone, D: inc parasymp

Kidney: (% use of body blood + oxygen) + (bloodflow)

25% Cardiac output

10% oxygen

Kidneys: GRF control

afferent arterioles -> glomeral capillaries -> efferent arterioles

How do NSAIDs and ACE 1 inhibitors / ARBs effect GFR?

Acute Kidney Injury (Basic def)

abrupt 48 hr decline in kidney function

→ accumulation of waste products

usually reversible

3 Indicators of Acute Kidney Injury (AKI)

inc serum Creatine (retained waste), oliguria (dec urine output), Azotemia (nitrogen in blood- BUN)

Risk factors for AKI

factors associated with aging: dec kidney volume (atrophy), arterial thickening, dec BF / GFR

*Cr levels can appear low/normal bc dec muscle mass

4 mechanisms that contribute to AKI

endi

endothelial injury (from vascular disturbances)

nephrotoxins

dec autoregulation

inflammatory mediators (imbalance → inc vasoconstriction)

List the 3 categories of AKI

Pre-renal (most common), Intrinsic (acute tubular necrosis, acute interstitial nephritis, contrast induced nephropathy), Post-renal (downsteam blockage)

Pre-renal AKI

Intrinsic AKI

structural damage to nephron

Acute tubular necrosis (ischemic/toxic death)

Acute Interstitial nephritis (inflam- allergic resp)

Contrast induced nephropathy

Post-renal AKI

abrupt BP inc

afferent dilate to compensate > underperfusion

efferent change to avoide damage

Chronic Kidney Disease (Basic def)

reduced function for 3 months

gradual/chronic glomerular damage

CKD steps (2) (+ term for turning point)

1) initiating mechanisms/damages, 2) progressive mechanism: trying/failing to fix (overwork/bail out)

little lady: “so how do we want to progress from here”

*renal progression: point at which remaining nephrons begin to die

Steps in End Stage Renal Failure *

persistent injury → HTN, Proteinuria, Sclerosis

proteinuria → mononuclear cell + cytochemokines → inflam

T lymphocyle activation → Synth pore forming proteins

mesenchymal transition → Fibrosis not functional

2 categories of Cerebrovascular Disease

ischemic: impaired BF/oxygenetation

hemorrhagic: BV rupture (aneurysm)

5th leading cause of death in US

cerebrovascular disease

3 Basic Processes / Ways Cerebrovascular Disease Occurs

1) thrombotic occlussion (blood clot)

2) emboolic occlusion (piece of clot)

3) vascular rupture (aneurysm)

Brain function: what is the limiting substance?

Oxygen

Cerebral bloodflow: consistency / control

remains constant over dif BP and intracranial pressure bc

autoregulation + vascular resistance