USMLE step 1 Pathology (Part 001)

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By: Qi Ke
Created: 2011-12-28
Size: 80 flashcards
Views: 91

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The causes of metastatic calcification (hypercalcemia)

Hyperparathyroidism
Bone destruction secondary to metastasis
Paraneoplastic syndromes
Vitamin D toxicity
Sarcoidosis
Chronic renal disease

Marasmus & Kwashiorkor

Marasmus: Decrease in total caloric intake.

Kwashiorkor: Decrease in total protein intake.

Cardinal signs of inflammation

Rubor=redness
Calor=heat
Tumor=swelling
Dolor=pain
Functio laesa=loss of function

The features of irreversible cell injury

Severe membrane damage.
Mitochondrial dysfunction.
Rupture of the lysosome.
Nuclear changes.

Pyknosis

Degeneration and condensation of nuclear chromatin.

Factors that increase vascular permeability

Histamine
Serotonin
Bradykinin
Leukotriene

Chronic granulomatous inflammation

Macrophages-->epithelioid cell-->multinucleated giant cell

lymphocytes and plasma cell

central caseous necrosis

Diseases: Tuberculosis, Cat-scratch fever, Syphilis, Leprosy, Fungal parasitic infection, Foreign bodies, Sarcoidosis(结节病).

Types of Necrosis

Coagulative (most common)
Liquefaction (abscesses, brain infarcts)
Caseous (tuberculosis)
Fat
Fibrinoid
Gangrenous (Dry/wet) Limbs, gallbladder, GI tract, testes

Function of complement

C5b-C9: membrane attack complex.

C3a, C5a: anaphylatoxin to release histamine.

C5a: leukocyte chemotactic factor

C3b: opsonin for phagocytosis

Chemotactic factors for NE

N-formyl-methionine

LTB4

C5a

IL-8

Liquefaction necrosis

Hydrolytic enzyme
Autolysis & Heterolysis
Abscesses, Brain infarct, Pancreatic necrosis

Arachidonic acid products

Cyclooxygenase

Thromboxane A2 [platelets]: 缩血管 & platelets aggregation.
Prostacyclin [vascular endothelium]: 扩血管 & inhibits platelets aggregation.
PGE2: Pain
PGE2, D2, F2: 扩血管

2. Lipoxygenase

LTB4: NE chemotaxis.
LTC4, D4, E4: 缩血管

Kinin system

Bradykinin: [liver]

Increase vascular permeability
Pain
Vasodilation
Bronchoconstriction

Features of reversible cell injury

Decreased oxidative phosphorylation

Decreased Na⁺K⁺ATP pump activity

Switch to glycolysis

Decreased protein synthesis

Plasma-membrane blebs & myelin figures.

Coagulative necrosis

Denaturing and coagulation of proteins

Loss of nucleus but preservation of cellular shape

Heat, liver, kidney.

Karyolysis

Dissolution of the nucleus

Vasodilatation factors

Histamine

Bradykinin

Prostaglandin

Karyorrhexis

Nuclear fragmentation

Vasoactive amines

Histamine

produced by basophils, platelets and mast cells

vasodilation, increase vascular permeablitiy.

induced by IgE reaction, injury, C3a C5a, IL-1

Serotonin

produced by platelets

same effect

Five processes of tissue repair

Hemostasis

Inflammation

Regeneration

Fibrosis--macrophages, granulation, type III collagen

Remodeling--macrophages, fibroblasts, type I collagen

Labile cells

Regenerate throughout life

surface epithelial cells, hematopoietic cells, stem cells

Stable cells

Replicate at a low level throughout life

Have the capacity to divide if stimulated

Hepatocytes

Permanent cells

Very low level of replicative capacity

Neurons and cardiac muscle

Growth factors and cytokines mediates tissue repair

Transforming growth factor (TGF-b)

Platelet-derived growth factor (PDGF)

Fibroblast growth factor (FGF)

Vascular endothelial growth factor (VEGF)

Epidermal growth factor (EDF)

Tumor necrosis factor (TNF-a) and IL-1

Primary union

Occurs with clean wounds when there has been little tissue damage and the wound edges are closely approximated

Surgical incision

Secondary union

Occurs in wounds that have large tissue defects and when the two edges of the wound are not in contact

requires large amount of granulation tissue

results in larger residual scars

Repair in specific organs

Liver: 1. hepatocytes. 2. regenerative nodules surrounded by fibrosis.

Brain: microglia remove debris and astrocytes proliferate.

Heart: fibrosis.

Lung: Type II pneumocytes.

Peripheral nerves: Distal part degenerates; proximal part regrows slowly

Wound Healing Processes

Day1, fibrin & inflammation cells. Day2-3, macrophages & granulation tissue. Day4-5, neovascularization. Week2, collagen. 1 month, dense collagen with remaining dilated blood vessels.

The final phase of wound healing, about one month.

Subacute infarction with granulation tissue formation containing numerous capillaries stimulated by vascular endothelial growth factor.

Causes of edema

increased hydrostatic pressure:充血性心衰,hypertension, renal retention

hypoalbuminemia:liver disease,肾病综合征

lymphatic obstruction

increased endothelial permeability,type I 超敏

increased interstitial sodium原醛,肾衰

Graves disease:pretibial myxedema,exophthalmos

Anasarca

extreme generalized edema, is a medical condition characterised by widespread swelling of the skin due to effusion of fluid into the extracellular space.

It is usually caused by liver failure or renal failure and severe protein deficiency.

Types of edema fluid

Transdudate:low protein,gravity<1.020

Exudate:high protein & cells,gravity>1.020,purulent,fibrinous,eosinophilic,hemorrhagic

lymphedema:non-pitting edema with protein-rich fluid

glycosaminoglycan-rich edema:increased hyaluronic acid

Hemostasis

sequence of events leading to the cessation of bleeding by the formation of a stable fibrin-platelet hemostatic plug

Platelets

1. platelets-Gp Ib-vWF-subendothelial collagen.

2. change shape, degranulation, thromboxane A2, phospholipid complex.

3. aggregation by thromboxane A2 & ADP, platelet-Gp IIb-IIIa-fibrinogen-Gp IIb-IIIa-platelet

normal: 15,000-400,000

Contents of platelet granules

Alpha granules:fibrinogen,fibronectin,factor V, vWF,platelet factor4,PDGF

Dense bodies:ADP,Calcium,Histamin,serotonin,epinephrine

Bernard-Soulier syndrome

Autosomal recessive

Deficiency of platelet Gp Ib

Devective platelet adhesion

Glanzmann Thrombasthenia

Autosomal recessive

Deficiency of Gp IIb-IIIa

Defective platelet aggregation

Platelet disorders

Thrombocytopenia

decreased production: aplastic anemia, tumer
increased destruction: ITP,TTP,DIC,hypersplenism

Qualitative defects

von Willebrand disease
Bernard-Soulier syndrome
Blanzmann thrombasthenia
Aspirin

Uremia

Immune thrombocytopenia purpura (ITP)

thrombocytopenia by IgG attack, resulting in petechiae, purpura, and a bleeding diathesis.

Type II 超敏, against Gp IIb-IIIa and Gp Ib-IX

Ab made in spleen and platelet destroyed by macrophages in spleen.

Forms of ITP

Acute: children following viral infection and self-limited.

Chronic: women in childbearing years, first manifestation of SLE, Petechiae, ecchymoses, menorrhagia and nosebleeds.

ITP lab

Decreased platelet count and prolonged bleeding time.

Normal PT and PTT

Peripheral blood smear: thrombocytopenia with enlarged megathrombocytes.

Bone marrow biopsy: increased number of megakaryocytes with immature forms.

Treatment of ITP

Corticosteroids: against Ab
Immunoglobulin therapy: flood Fc receptor
Splenectomy

Thrombotic thrombocytopenic purpura (TTP)/HUS

deficieny/inhibition of ADAMTS13, which leaving multimers of vWF.

adult women, fever, thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms, 肾衰

platelet thrombi with fibrin

schistocyte and reticulocytosis in peripheral blood smear

Prothrombin time PT

tests the extrinsic and common coagulation pathways (7,10,5,2,1)

Internatiional normalized ration (INR)

Partial thromboplastin time PTT

tests the intrinsic and common coagulation pathways(12,11,9,8,10,5,2,1)

Thrombin time TT

tests for adequate fibrinogen levels (1)

Fibrin degradation products FDP

tests the fibrinolytic system (decreased with DIC)

Hemophilia A

Deficiency of factor VIII, X-linked recessive, Males

spontaneous hemorrhages in joints

easy bruising and hematoma formation

prolonged bleeding after surgery

no petechiae or ecchymoses

Lab: prolonged PTT

Treatment: factor VIII concentrate

Hemophilia B (Christmas disease)

Deficiency of factor IX

X-linked recessive

identical to hemophilia A

Acquired coagulopathies

Vitamin K deficiency: decreased factors 2,7,9,10, and protein C & S

Liver disease: decreased synthesis of all clotting proteins

Von Willebrand disease

inherited deficiency of defect in vWF

produced by endothelial cells or megakaryocytes.

spontaneous bleeding from mucous membranes.

prolonged bleeding, menorrhagia

prolonged bleeding time, PTT

Abnormal platelet response to ristocetin

treatment: desmopressin

DIC

Obstetric complications

Gram-sepsis

Microorganisms

AML M3

Adenocarcinomas

widespread microthrombi, consumption of platelets and clotting factors

Decreased platelet count, prolonged PT/PTT, decreased fibrinogen, elevated D-dimer

Treatment: underlying disorder

Thrombosis

Pathologic formation of an intravascular fibrin-platelet thrombus during life.

Factors involved in thrombus formation (Virchow's triad)

Endothelial injury: atherosclerosis
Alterations in laminar blood flow: stasis,turbulence,hyperviscosity
Hypercoagulability: clotting disorders, tissue injury, neoplasia, nephrotic syndrome, age, pregnancy, oral contraceptives

Embolism

any intravascular mass that has been carried down the bloodstream from its site of origin, resulting in the occlusion of a vessel

Composition of emboli

Thromboemboli

Atheromatous emboli

Fat emboli

Bone marrow emboli

Gas emboli

Amniotic fluid cmboli

Tumor emboli

Talc emboli

Bacterial/septic emboli

Pulmonary emboli (PE)

95% arise from DVT, pelvic venous plexuses of the prostate and uterus, right side of the heart.

V/Q mismatch, DVT in leg veins, elevated D-dimer

75% no sequelae

15% infarction, SOB, hemoptysis, pleuritic chest pain, pleural effusion

5% sudden death

Paradoxical emboli

any venous embolus that gains access to the systemic circulation by crossing over from the right to the left side of the heart through a septal defect.

Infarction

ischemia->necrosis

thrombotic or embolic occlusion, vasospasm, torsion of vessel.

sites: Heart, brain, lung, intestine, kidney

wedge shape point to the occlusion

anemic infarct,white,spleen, kidney,heart

hemorrhagic infarct,red,lung,intestine

necrosis

Shock

vascular collapse and widespread hypoperfusion of cells and tissue due to reduced blood volume, cardiac output, or vascular tone

Causes of shock

Cardiogenic shock: infarction, arrhythmia, PE, cardiac tamponade

Hypovolemic shock: hemorrhage, burn, dehydration

Septic shock: gram-septicemia, endotoxin in circulation

Neurogenic shock: anesthesia, brain injury

Anaphylactic shock: Type I 超敏

Stages of shock

compensation: sympathetic tone, catecholamine, renin-angiotensin system
decompensation: decreased tissue perfusion, reversible injury, lactic acidosis, electrolyte imbalances, renal insufficiency
irreversible: organ failure, death

Nutmeg liver caused by chronic passive congestion.

Thrombolytic therapy

Tissue plasminogen activator is a thrombolytic agent that causes the generation of plasmin, which cleaves fibrin to dissolve clots.

Disorders involving an extra AUTOSOME

1. Down syndrome (trisomy 21)

2. Edwards syndrome (trisomy 18)

3. Patau syndrome (trisomy 13)

Disorders involving CHROMOSOMAL DELETIONS

1. Cri du chat syndrome (猫叫综合征) 46 XX or XY, 5p-

2. Microdeletions

Disorders involving SEX CHROMOSOMES

1. Klinefelter syndrome (47 XXY)

2. Turner syndrome (45XO)

HERMAPHRODITISM

1. Female pseudohermaphroditism (46XX)

2. Male pseudohermaphroditism (46XY)

AUTOSOMAL recessive disorders

1. Cystic fibrosis (mucoviscidosis)

2. Phenylketonuria (PKU)

3. Alkaptonuria (ochronosis)

4. Albinism

5. Glycogen storage diseases

6. Tay-Sachs disease

7. Niemann-Pick disease

8. Gaucher disease

9. Mucopolysaccharidosis (MPS)

AUTOSOMAL dominant disorders

1. Familial hypercholesterolemia

2. Marfan syndrome

3. Ehlers-Danlos syndrome (EDS)

4. Neurofibromatosis

5. von Hippel-Lindau disease

X-linked recessive conditions

1. Lesch-Nyhan syndrome

2. Testicular feminization

3. Chronic granulomatous disease

4. Bruton agammaglobulinemia

Triplet repeat mutations

1. Fragile X syndrome

2. Huntington disease

Genomic imprinting

Def: differential expression of genes based on chromosomal inheritance from maternal versus paternal origin.

1. Prader-Willi syndrome

2. Angelman syndrome

Mitochondrial DNA disorders

Def: mitochonfrial DNA codes for mitochondral oxidative phosphorylation enzymes; inheritance is only from mother to child, because only the ovum contributes mitochondria to the zygote.

1. Leber hereditary optic neuropathy

2. Myoclonic epilepsy

Multifactorial inheritance

Def: disease caused by a combination of multiple minor gene mutations and environmental factors.

1. neural tube defects and type 2 diabetes mellitus

47 XX or XY +21 1/700

retardation, mongoloid facial, brushfield spots, hypotonia, broad short neck, palmar crease, endocardial cushion defect, duodenal atresia, hirschsprung, ALL, Alzheimer disease
甲胎, chorionic gonadotropin and unconjugated estriol.

47 XX or XY +18

retardation, low-set ears and micrognathia, heart defects, overlapping flexed fingers, Rocker-bottom feet
very poor prognosis

47 XX or XY +13

retardation, cleft lip palate, heart defects, renal abnormalities, microcephaly, polydactyly, microphthalmia
very poor prognosis

About this deck

By: Qi Ke
Created: 2011-12-28
Size: 80 flashcards
Views: 91

About StudyBlue

“I have used this website for three exams, and I see a huge difference in my test results.”
Naj