Boards: Pathology

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Hematoxylin

Part of H & E stain

Stains the following structures blue to purple:
Nuclei
Nucleoli
Bacteria
Calcium

Eosin

Part of H & E stain

Stains the following structures pink to red:
Cytoplasm
Collagen
Fibrin
RBC's
Thyroid Colloid

FIGURE: Overview of the ETC

What are the inheritance patterns of proteins in regard to pathology?

Genetic defects in enzymes are usually RECESSIVE

Genetic defects in structural proteins are usually DOMINANT

Vitamin A Deficiency

Night Blindness
Squamous Metaplasia
Immune Deficiency

"Battling cancer, Bugs Bunny is sick and weak, trying to find his carrots in the dark."

Vitamin C Deficiency

Scurvy

Vitamin D Deficiency

Rickets
Osteomalacia

Vitamin K Deficiency

Bleeding Disorder

Vitamin B12 Deficiency

Megaloblastic Anemia
Neuropathy
Spinal Cord Degeneration

Folate Deficiency

Megaloblastic Anemia
Neural Tube Defects

Niacin Deficiency

Pellagra (diarrhea, dermatitis, dementia)

What are protective factors against Free Radicals?

1. Antioxidants, Vitamins A, E, C

2. Superoxide dismutase (turns superoxide --> hydrogen peroxide)

3. Glutathione peroxidase (Turns hydrogen peroxide or hydroxl ions --> water)

4.Catalase (turns hydrogen peroxide --> Oxygen and water)

FIGURE: Cellular Damage w/ MI

What are enzymatic markers for cell death?

MI (Heart): Creatinine phosphokinase-MB isoenzyme, Lactate Dehydrogenase, Troponin

Hepatitis (Liver): Transaminases

Pancreatitis: Amylase and Lipase

Biliary Tract Obstruction: Alkaline Phosphatase

What are the different types of necrosis?

COAGULATION
MC; in heart, liver, kidney; nucleus gone but shape intact

LIQUEFACTION
Autolysis and heterolysis from hydrolytic enzymes; ABSCESSES, brain infarcts, pancreatic necrosis

CASEOUS
Coag & Liq; Cottage cheese like; e.g. Tb

FAT
Lipases; Grossly chalky appearance (from FA assoc w/ calcium)

FIBROID
Looks like fibrin; stains pink

GANGRENOUS
Dead tissue; Usually in Lower limbs, GB, GI tract, testes; can be wet (Liq) or dry (Coag)

What are the 5 cellular adaptive responses to injury?

1. Atrophy (shrink)

2. Hypertrophy (grow)

3. Hyperplasia (multiply)

4. Metaplasia (reversibly change)

5. Dysplasia (abnormal)

Pro-inflammatory Amines

HISTAMINE -> Vasodilation and Inc. vasc. perm.
Made by Basophils, platelets, Mast Cells

SEROTONIN -> Vasodilation and Inc. vasc. perm.
Made by platelets

Pro-inflammatory Kinin System

Activated Factor XII (Hageman) turns Pre-kallikrein --> kallikrein

Kallikrein turns kininogen --> bradykinin

BRADYKININ -->Pain, Vasodilation, Bronchoconstriction, Inc. vasc. perm.

Two major Arachodonic Acid Pathways

CYCLOOXYGENASE (COX)
Thromboxane
Prostacyclin
Prostaglandin

LIPOOXYGENASE
Leukotrienes

Mediators of Pain

Bradykinin

Prostaglandins (E2)

Mediators of Fever

IL-1
IL-6
TNF-alpha
Prostaglandins

What are the 2 types of multi-nucleated giant cells? How are they different?

Langerhans-type giant cell
Peripheral nuclei

Foreign Body giant cell
Haphazard nuclei (like foreign drivers, all over the place)

What are the 5 types of Histological patterns in infected tissue?

The Munsters

EXUDATIVE inflammation (Marilyn, pretty ordinary)
acute response w/ neutrophils

NECROTIZING inflammation (Herman, Frankenstein, dead body)
severe cell damage and extensive death

GRANULOMATOUS inflammation (Grandpa)
granulomatous response; usually slow growing

INTERSTITIAL inflammation (Lilly)
lots of mononuclear cells; usually viral

CYTOPATHIC/CYTOPROLIFERATIVE inflammation (Eddie, changes around into wolfman)
Infected/injured cell is altered

Chediak-Higashi Syndrome

...

What are the different types of collagen?

I (ortho's #1) -> Common; skin, bone, tendons, most organs

II (you have 2 ears and eyes) -> Cartilage and vitreous humor

III (babies and scars) -> granulomatous tissue, embryonic tissue, uterus, keloid

IV (on the floor) -> Basement membranes

Name the 3 collagen deficiencies.

Scurvy -> Vitamin C def, bleeding gums

Ehlers-Danlos Syndrome

Osteogenesis Imperfecta (Mr. Glass) -> Type 1

Difference between transudate vs. exudate

TRANSUDATE -> edema fluid w/ LOW protein content

EXUDATE -> edema fluid w/ HIGH protein content, can be pustular, fibrous, bloody, eosinophilic

Bernard-Soulier Syndrome

Autosomal Recessive
Deficiency in Platelet Gp Ib
Defective platelet adhesion

Glanzman Thromasthenia

Autosomal Recessive
Deficiency in Platelet Gp IIb-IIIa
Defective Platelet aggregation

Immune Thrombocytopenia Purpura

Spleen makes ANTIBODIES to platelet antigens

Acute --> can follow infection
Chronic --> can follow autoimmune disease

Prolonged BLEEDING TIME
Normal PT & PTT

Tx --> Corticosteroids, Splenectomy, Ig Therapy

Thrombitic Thromocytopenia Purpura

Begins with several clots forming in small vessels --> leads to hemolysis and schistocyte formation

PENTAD of signs: Thrombocytopenia, Fever, Neuro problems, Anemia, Renal Failure

Hemolytic Uremic Syndrome (HUS)

Commonly occurs in children following gastroenteritis w/ bloody diarrhea (E. coli)

PENTAD of signs: Thrombocytopenia, Fever, Neuro problems, Anemia, Renal Failure

Prothrombin Time

Tests the extrinsic pathway (PeT)

VII, X, V, prothrombin (II), fibrinogen (I)

Partial Thromboplastin Time

Tests the intrinsic pathway (PiTT)

XII, XI, IX, VIII, X, V,prothrombin (II), fibrinogen (I)

Hemophilia A

X-linked recessive

Deficiency of Factor VIII

No petichiae or ecchymoses

Normal Bleeding time, PT
PROLONGED PTT

Most common sites for infarction from systemic arterial emboli

Lower Extremities
Brain
Kidneys
Intestine
Spleen

Paradoxical emboli -> cross from right to left via septal defect

What is the difference between an anemic infarct and a hemorrhagic infarct?

ANEMIC (pale or white color)
Occurs in solid organs w/ single blood supply
e.g. -> Kidney, Spleen, Heart

HEMORRHAGIC (red)
Occurs in organs w/ dual or collateral blood supplies
e.g. -> Lung, Intestines, Testes (w/ torsion)

What are the stages of shock?

I -> Compensation (maintain as much perfusion to organs)
Increased symp. tone, Adrenergic Activation, RAAS activation

II-> Decompensation (decrease in perfusion)
Reversible injury occurs, Metabolic acidosis, electrolyte imbalances, renal insufficiency

III -> Irreversible
Irreversible tissue injury and organ failure -> DEATH

Glycogen Storage Diseases

Autosomal Recessive

A deficiency in an enzyme that breaks down glycogen --> it accumulates in the LIVER, HEART, SKEL MUSC

Lysosomal Storage Diseases

Autosomal Recessive

A deficiency in lysosomal enzymes --> accumulate different kinds of substrate that should have been broken down

There are several types and they often have CNS effects

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