patho final exam

Four types of intracellular accumulations that can lead to injury?

• Excess normal substances

• abnormal substances (faulty metabolism/protein misfolding)

• pigments

• particles cells can’t degrade

Most common cause of cell injury?

Ischemia

• restricts blood flow, injures cells faster than hypoxia, may be reversible early.

Tissue hypoxia results in what main cellular problem?

Power failure in the cell → ATP depletion

When does anaerobic respiration begin and its consequences?

Starts when O₂ is lacking → lactic acid buildup, pain, fatigue, less ATP.

Mechanisms of reperfusion injury?

• Calcium overload

• free radicals

• inflammation

Mechanism of radiation injury?

• Heat

• radiolysis

• free radical formation.

Two types of reversible cell injury?

hydrophobic swelling & intracellular accumulation

hydrophic swelling

Na⁺/K⁺ pump failure, water entry

intracellular accumulation

fat, pigments, misfolded proteins

How are misfolded proteins handled in cells?

Chaperones refold, translation decreases, ubiquitin tags for proteasome degradation, caspases trigger apoptosis

atrophy

decrease cell size and function

• from disuse, denervation, ischemia, starvation, persistent injury

hypertrophy

increase cell size

• from demand or increased protein content

hyperplasia

increase cell number

• from hormonal stimulation or chronic irritation

metaplasia

Reversible cell type change

• example: Barrett’s esophagus.

dysplasia

Disorganized growth

• pre‑cancerous.

Most common type of necrosis

Coagulative necrosis

• ex: heart (ischemia).

Liquefactive necrosis

Tissue dies and turns into a soft, liquid-like goo because enzymes break it down

• ex: brain - enzymatic digestion, cyst/abscess.

fat necrosis

Fat tissue breaks down into oily, chalky lumps after injury or inflammation

• ex: pancreas - chalky white deposits

caseous necrosis

Tissue looks soft, white, and cheesy—usually caused by tuberculosis infection

• ex: Lung in TB — clumpy cheese appearance.

Three gangrene types

• Dry (coagulative)

• wet (liquefactive + infection)

• gas (Clostridium, gas bubbles).

apoptosis

Programmed cell death without inflammation

extrinsic apoptosis

death receptor signals

intrinsic apoptosis

p53 response to DNA damage.

Common side effects of chemotherapy

Anemia, nausea, bleeding, infections

• from bone marrow suppression and poor nutrition

leukopenia

• low wbc

• immunocompromised

• joint swelling

• weight loss

• hepstomeagly

• splenomeagly

thrombocytopenia

low platelet from bone marrow

• predisposed to hemorrhage

• petechiae, bruising, bleeding gums

benign tumor

• same tissue as tumor location

• slow growth

• encapsulated

• rare recurrence

malignant tumor

• rapid growth

• common reoccurrence

• metastasizes

• necrorsis common

• invasive

-oma

indicated benign tumor

• except: lymphoma, heptatoma, melanoma

-carcinoma

epithelial origin

-sarcoma

connective (mesenchymal origin)

• nerve, bone, muscle

proto-oncogenes

promote normal growth

• mutate into oncogenes

tumor suppressor gene (p53 & Rb)

inhibit cell proliferation

• loss = uncontrolled growth

p53

most common tumor suppressor

• inhibits cell cycle

• allows DNA repair or apoptosis if severe damage

RB gene

blocks cell division

• binds to transcription factors & inhibits transcribing genes

BRCA1 & BRCA2

breast cancer

• when loss of function

common cancer causing viruses

• HIV

• EBV (Burkitt lymphoma)

• HTLV-1 (adult T cell leukemia/lymphoma)

• Hep C

HIV

kaposi sarcoma

EBV

Barr virus

• Burkitt lymphoma

HTLV‑1

adult T‑cell leukemia/lymphoma

grading

microscopic anaplasia level (1–4)

staging (TNM)

• T: tumor size and location

• N: nodes

• M: metasasis

Cancer cachexia

• weight loss

• weakness

• anorexia

• nausea & vomiting

Neutropenia

• low neutrophil count < 500 cells/μL

• increases infection risk

Hypersensitivity

Normal immune response that is inappropriately triggered/excessive

Type I hypersensitivity

• IgE mediated

• immediate (allergy, anaphylaxis, asthma)

type I hypersensitivity treatments

• Ige blocker

• antihistamines

• epinephrine

• corticosterioids

• anticholongerics

epinephrine

counter histamine (epipen)

beta adrenergic

bind to beta adrenergic receptors and prevent catecholines from binding

corticosteroids

decrease inflammation by binding to glucorticoid receptors in cytoplasm

Type II hypersensitivity

• cytotoxic or IgG/IgM (principle antibodies) mediated (cells will die)

• antibodies attack antigens on surface

• mismatched transfusion

• hemolytic newborn disease (Rh- and Rh+)

Type III hypersensitivity

immune complex deposition > tissue damage

• lupus, arthritis, post strep glomerulonephritis

Type IV hypersensitivity

t-cell delayed

• tb test, contact dermatitis, type 1 diabetes

Common autoimmune disease treatments?

Immunosuppressants, corticosteroids, plasmapheresis.

mutation in “blast” = acute leukemia

• bone marrow filled with immature blast > 20% (normally 3-4%)

• blast spilled over to bloodstream > 10% (0.1 - 0.4%)

mutation in “functional cells” = CHRONIC leukemia

• bone marrow = normal cells & mutated cells

• found accidentally

chronic myeloid leukemia (CML)

• 40 - 50 yo

• philadelphia chromosome (bcr/abl fusion): translocation of chromosome 9 and 20

• high granulocytes

• treat with anti‑bcr/abl therapy

• poor chemo response.

acute myeloid leukemia (AML)

• most adults; median age 64 yo

• > 20% blasts in BM

• prognosis worse for AML than ALL

chronic lymphoid leukemia (CLL)

• most COMMON leukemia

• 95% are malignant B-cell precursors

• 5% aggressive T-cell transformation

• asymptomatic until fatigue, weight loss

• infection; lymph node/spleen enlargement, anemia, bleeding.

acute lymphoblastic leukemia (ALL)

• ALL children 3 - 7 yo OR middle aged adults

• hemarthrosis among children - refuse to walk

• better prognosis in children than adults

• abrupt bone pain, bruises, fever, fatigue, hepatosplenomegaly, lymphadenopathy.

hemarthrosis

bleeding pools in joint cavity

• can be a sign of hemophilia

aplastic anemia

stem cell disorder - where the body stops making enough red blood cells, white blood cells, and platelets

cause of aplastic anemia

toxins, radiation, and immune injury

treatment for aplastic anemia

bone marrow transplant & immunosuppressants

anemia of chronic renal failure

Low red blood cell count - diseased kidneys not making enough erythropoietin (the hormone that tells bone marrow to make RBCs)

treatment for anemia of chronic renal failure

• dialysis erythropoietin

• iron

• folate

• B12

B12 deficiency anemia

Body can’t make enough healthy red blood cells due to low vitamin B12

• causes large RBCs (↑ MCV), fatigue, and nerve problems.

• poor diet or lack of intrinsic factor (pernicious anemia).

treatment for B12 anemia

vitamin B12 or folic acid

iron deficiency anemia

Low iron → body can’t make enough hemoglobin → small, pale RBCs

iron deficiency anemia causes

fatigue, weakness, and pale skin; often from blood loss or poor diet.

treatment for iron deficiency

Iron supplements (pills or IV) and treating the cause of low iron, like blood loss or poor diet.

thalassemia

inherited blood disorder where the body makes abnormal hemoglobin

• causes RBCs to be small, fragile, and break apart easily → anemia.

treatment for thalassemia

blood transfusion, bone marrow transplant

sickle cell anemia

Inherited disorder where RBCs become stiff and crescent‑shaped, blocking blood flow

• pain, anemia, and organ damage

sickle cell anemia treatment

bone marrow transplant

Hemolytic disease of newborn

Rh incompatibility → hemolysis, severe jaundice, cyanosis