patho test 1

oh my good lord

atrophy

cells shrink. caused by disuse, lack of innervation, lack of endocrine stimulation, malnutrition, ischemia

Hypertrophy

increase in cell size, results from increase in workload-most often cardiac and skeletal muscles. can be normal or pathological-such as heart walls thickening making it harder to pump blood

Hyperplasia

increase in cell number, Caused by gene activation and presence of intracellular messengers that control rep and growth= most often due to a stressor like pregnancy or warts 

metaplasia

reversable change, when one cell type is replaced w another. mostly pathological, like smokers lungs

dysplasia

deranged cell growth of a specific tissue.

pathological calcifications

dystrophic (bad growth of calcium), metastatic (cancer in the bones), abnormal tissue deposits from age or bed rest

free radicals

unpaired electron build up. Can be from drugs, radiation, or ischemia-reperfusion injury. Damages DNA, lipid membranes, oxidative modification of proteins=cell death

Recipe for inflammation

Endothelial cells (blood vessel): get leaky and release chemicals and wbcs

platelets: thrombocytes, clot blood

leukocytes: wbcs, first responders→ adaptive immunity

Vascular Stage of Inflamm

Capillary microcirculation: endothelial cells spread, get leaky, allowing wbcs and chemical mediators to get to the tissues. Blood gets thicker to trap microbes

Cellular Stage of Inflammation

Margination: white blood cells move outside of capillaries and cross endothelium, organized by chemotaxis

Arachidonic acid pathway:

• Lipoxygenase: makes leukotrienes that causes smooth muscle contraction and leaky vessels

• Cyclooxygenase pathway (aspirin, nsaids block this) creates prostaglandins (vasodilation, inhibits inflammatory cell function, pain)  and thromboxane (constriction, promotes platelet function, why ibuprofen causes bleeding) 

Systemic signs of inflamm

• Lymphadenopathy/ swollen lymph nodes

• Inflammatory mediators being released in circulation

• lead to reactions in the lymph system. 

Acute phase response: what does the liver synthesize?

Fibrinogen: plasma protein, creates mesh to repair tissue

CRP: nurses measure this to find localized inflammation

Amyloid A: elevated during chronic inflammation

What is the normal range of WBCs

4000-10000

Type one hyper sensitivity:

IgE mediated

RAPID'

Granuolcyte involvement: mast in CT and baso in bloodstream

1st exposure: IgE creation in repsponse to the allergen, no symptoms

2nd exposure: IgE aggregates

Histamine and Heparin: cellular response

Anaphylaxis

SS: vasodilation, hypotension, arterial hypoxia, airway edema

TX:  remove allergen, protect airway, iv, volume resuscitation, epinephrine

Atopic Type 1:

• Urticarial rash (hives), allergic rhinitis, atopic dermatitis, bronchial asthma

Risk factors: type 1

• asthma, adolescents, family history

• Degree of reaction depends on amount, empty stomach, concurrent illness/medication, exercise, menstrual cycle

Type 2

-Antibody mediaited/cytotoxic

-IgG and IgM

-intrinsic or extrinsic antigens

-Blocks recpetors

type 3

IgG and IgM mediated

Formation of antibody/antigen complexes in blood stream= activates compliment cascade

often end-organ vessels: skin, kidney, etc

Arthus rection vs Serum Sickess

Serum: systemic, generalized tissue damage and edema, rash, fever, lymph

Arthus: local; lesions, tissue necrosis, localized vasculitis

Type 4

DELAYED: mild to severe based on amount of exposure. Memory T cells formed upon first exposure-delayed response after second.

Allergic Contact Dermatitis

Sensitization and elicitation phases- type 4

Direct skin contact with hapten

associated w latex allergies, poison ivy, etc

Hypersensitivity Pneumonitis

Inflammatory lung disease-type ¾

Characterized by repeated inhalation of allergen. Hours after exposure resp symptums

Acute Hemolytic transfusion

-ABO compatibility, type 2

-PREVENTION IS KEY

-Kidney failure in worst cases bc of hg deposits

Delayed Hemolytic

Occurs weeks after transfusion, mix of type four and two

Jaundice or asymptomatic

Febrile Reaction

-When donor white blood cells react with recipient antibodies

-Fever developed in hours bc of IL and TNF releases

-Leukocyte reduced blood may be neccesary

Transfusion related Acute Lung Injury

Rare, Human leukocyte antigen in donor blood

• within 6 hours, pulmonary edema, hypotension, hypoxemia 

GVHD-General

Graft has immune cells capable of functioning+recipent expresses antigens not present in donor cells+recipient is immunologically comp in some way=GVHD

Human Leukocyte Antigens must be as close as possible for allogenic donations

Acute GVHD

Recipient makes APCs, donor T cells proliferate and attack tissues, mediators begin a compliment cascade.

ss: first 100 days post transplant, skin palp rash, GI Ulcers, liver toxicity

Chronic GVHD

Older individuals, previous acute, major cause of late death after chemo on bone marrow

Albumin

Normal: 3.5-5

Purpose: keeps fluid in the vessel, regulates oncotic pressure, related to protein nutritional status

Edema Formation

swelling occurs when vascular fluid moves to interstitial spaces

Dependent edema: gravity pushing fluid out, ie sitting to long and ur feet swell

Low albumin: liver failure, kidney loss, or burns

Obstructed lymph flow

Effects of Edema:

-life threatening in brain, lungs, layrnx

-Impaired function of extremities and joints

-Tissues have difficulty getting o2 and nutrients

-compresses vessels

Transcellular space edema

-closly linked with lymphatics

-Burns, cancer, sirs, liver failure-hypoalbuminemia, ascites (peritoneal) →pleural effusion

How is water/na volume regulated

-Both from diet, both controled by kidneys

-Baroreceptors- respond to vessel walls stretching

-RAAS system-kidney pressure receptors

-ADH controls thirst-hypothalamus

Hypodipsia

Results from hypothalamus lesions, subarachnoid hemorrhages, or age. Decreased ability to sense thirst.

Polydipsia

can be symptomatic from fluid loss, congestive heart failure, CKD, Diabetes

Diabetes Insipidus

SS: excessive thirst, pee 3-30 L of urine a day. Cannot concentrate urine during water depletion.

Neurogenic: ADH synth/release issue

Nephrongenic: kidneys fail to respond to ADH

Can be caused by lithium, genetics, or electrolyte disordders

TX: 24 hour urine collection

Syndrome of Inappropriate ADH

-Dilution hypoatremia from H20 Retention

-Can be from surgery, drugs, stress pain or from lung lymph prostate pancreas produced ADH, tb/pnemonia, or CNS pressure

DX Of syndrome of innappropriate ADH

Na in urine greater than 20,

Urine osmolality> plasma osmolality,

abscense of edema

Normal renal, thyroid, and adrenal function

Hypovolumia-Isotonic Volume deficit

-low circulating ECF volume

-SS: weight loss, thirst, low intersticial and vascular volume=thready pulse, postural hypotension, pinch skin (turgor)

-Causes: decreased intake, kidney disease, diruetic therapy, sweating, burns

Hypervolumia-Isolotinic Volume Ecesses

-high circulating ECF

-SS: weight gain, edema, venous pressure, respirotary crackles and productive cough, hypertension and bound pulse

Causes: mostly kidney issues (renal failure), heartf failure, liver aldosterone failure, coricosterioids

Hypoatremia

-less than 135 na in plasma, h20 leaves ICF

-Hypotonic: Shift from ICF to ECF

-Hypovoluemic: diarhea, dehydration, adrenal issues, in babies bad formula ratio

-Normovolumemic: From SIADH

-Hypervolumic: heart failure, advanced liver disease, kidney failure

SS: fingerprint edema on stomach, neurological, muscle cramps, fatigue, stupor, coma

Hypernatremia

Na greater than 145, serum osmolaity greater than 295

Cause: dehydration from fever, GI issue, excess urine, tube feedings w/o proper hydration, rapid ingestion of na

SS: weight loss, hypotension, rapid pulse, warm skin, decrease urine output

Potassium:

3.5-5 is normal range

Get from diet, stored in rbcs, muscles, liver, bones

Function: resting membrane potential, acid base balance, metabolism, nerve impulses

Hypokalemia

• Causes:

  • Inadequate intake

  • Excessive renal loss (diuretics, corticosteroids)

  • GI losses

  • Transcompartmental shift

• Manifestations:

  • Serum K+ < 3.5 mEq/L

  • Muscle weakness, cramps

  • Fatigue, lethargy

  • Cardiac dysrhythmias

  • polyuria, glucose intolerance

  • Possible paralysis in severe cases

Hyperkalemia

• Definition: K+ > 5.5 mEq/L,

• Causes:

  • Excessive intake (diet, supplements, IV)

  • Tissue trauma, burns, etc

  • Inadequate renal elimination

• Symptoms:

  • Paresthesia (tingling, numbness)

  • Nausea, vomiting, weakness

  • Cardiac arrhythmias

  • RISK OF CARDIAC ARREST

• Tx

  • Sodium bicarbonate (NaHCO₃)

    Insulin + glucose

    β-adrenergic agonists

  • Remove excess K+: Diuretics, dialysis, potassium binders

Hypocalcimia

• Normal Range: 8.5-10.5 mg/dL

• Causes:

  • intake/vitamin D defecient

  • Hypoparathyroidism

  • Renal failure

  • Acute pancreatitis

  • Increased phosphorus levels

• Symptoms:

  • Chvostek's Sign: Tap below the temple near the facial nerve → facial spasm (lip, nose, face)

  • Trousseau's Sign: Inflate BP cuff above systolic pressure for 3 minutes → contraction of fingers and hand (tetany)

  • Muscle cramps, tingling (paresthesia), seizures, arrhythmias

• Causes:

  • Milk-Alkali Syndrome: Excessive ingestion of milk and antacids

  • Increased Bone Resorption: parathyroid hormone (PTH), cancer, or immobilization (bed-bound patients)

• Manifestations:

  • Polyuria

  • GI Issues

  • Muscle Weakness & Atrophy

  • Osteopenia & Osteoporosis (bone loss)

  • Neurological: Lethargy, personality changes, stupor, coma

  • Hypertension

Hypophosphatemia

• Normal Value: 2.5–4.5 mg/dL

• Causes:

  • Decreased Absorption: Antacids, diarrhea, lack of vitamin D

  • Increased Renal Elimination: Alkalosis, hyperparathyroidism, diabetic ketoacidosis

  • Malnutrition: Alcoholism, hyperalimentation, insulin during diabetic ketoacidosis recovery

• Manifestations:

  • Muscle aches, tremors, seizures, coma

  • Muscle weakness, bone pain

  • Hemolytic anemia, platelet dysfunction

Hyperphosphatemia

• Causes:

  • Renal Dysfunction: Kidney failure impairs phosphate elimination

  • Phosphate Overload: Excessive intake (laxatives, enemas, IVs with phosphate)

  • IC to EC Shift: Trauma, strokes, seizures

• Manifestations:

  • Cardiovascular and muscle issues

  • Low calcium levels

Hypomagnesemia

• Normal Value: 1.8–2.3 mg/dL

• K+ and Ca++ Depend on Magnesium

• Causes:

  • Malnutrition, small bowel bypass surgery, diuretic therapy

• Manifestations:

  • Athetoid movement (slow writhing movements)

  • Choreiform movement (cannot sit still)

  • Risk for osteoporosis, osteomalacia

Hypermagnesemia

• Causes:

  • Excessive intake (oral magnesium supplements)

  • Decreased excretion (renal failure)

• Manifestations:

  • Serum levels > 3 mg/dL

  • Lethargy, hyporeflexia, confusion

  • Cardiac issues, including cardiac arrest

  TX: Administer calcium

Hypercoagulability

• Causes:

  • Increased Platelet Function (normal 150k to 450k)

  • Accelerated Coagulation Cascade

• Types of Thrombi:

  • Arterial Thrombi: Platelet aggregates due to high-pressure turbulence

  • Venous Thrombi: Platelet and fibrin complexes due to slow blood flow

Thrombocytosis

• Platelet count >1 million/µL

• Causes:

  • Primary (Essential): Myeloproliferative disorder in bone marrow

  • Secondary (Reactive): Disease stimulating thrombopoietin production (e.g., tissue damage, infection, cancer)

• Manifestations:

  • Increased clotting, leading to thrombosis

  • Potential for hemorrhage (platelets used for clots, reducing circulation for bleeding control)

Thrombosis Clinical Manifestations-Primary

• Deep vein thrombosis, pulmonary embolism, Portal/hepatic vein 

• Hemmrohage: using up platelets for clots, none circulating to help stop bleeding, excess 

• Ethromelagia: painful throbbing in fingers because platelet aggregates block arterioles 

• Long asymptomatic periods followed by thrombotic episodes or hemorrhagic 

Thrombophillia

Inheritied thrombosis- high morbidity

Venous Stasis Thrombosis

• Caused by: Prolonged bedrest, immobility, myocardial infarction, cancer, hyper estrogenic states (pregnancy), smoking, obesity, oral contraceptives

  • Result: slow flow, venous congestion, hyperviscosity syndromes (polycythemia), increased resistance to receptors-> deformed RBVS and sickle cells 

  • Prophylaxis is KEY: miminizes morbidity heparins, abulation, movement, compression pumps on legs, 

Thrombocytopenia: 

platlet count less than 150k

-Bone marrow loss (aplastic anemia) from:

• Radiation/drug therapies 

  • Drugs like asprin induce ig/ab complex

• HIV infection

• Cytomegalo virus infection 

-Spleenomegaly- excessive pooling

-Mechanical injury from heart valves

-DIC when body uses all platlets

-Reduced Platelet survival from antibodies

Heparin-Induced Thrombocytopenia (HIT)

• Cause: Immune reaction against the complex of heparin + platelet factor 4 (PF4).

• Mechanism: Heparin binds to PF4, creating a complex that triggers an immune response. This activates remaining platelets, leading to thrombosis (clot formation).

• Consequence: As platelets are used in clotting, their count drops, increasing the risk of bleeding.

Primary Immune Induced Thrombocytopenia

• Primary: 

  • Autoimmune disease

    Secondary: reaction to disease like h pylori

  • Direct destruction of platelets 

  • Immune system inhibits formation

  • Idiopathic (dont knwo why it starts) 

• Clinical Manifest:

  • History of bruising

  • Platlet 20-30k

  • Gums bleeding

  • Epistaxis: nose bleed

  • Abnormal menstrual bleeding

  • Splenomegaly

  • Melena

Thrombotic Thrombocytopenic Purpura (TTP)

• Deficiency of ADAMTS13 gene leading to unchecked platelet aggregation.

• Manifestations:

  • Thrombocytopenia, hemolytic anemia, renal failure, fever, neurological abnormalities.

  • Purpura, petechiae rash, vaginal bleeding, headache, seizures, altered consciousness.

• Treatment: Plasmapheresis (remove plasma and replace with frozen plasma)

Coagulation Factor Deficiencies

• Cause: Deficiency or impaired function of clotting factors (inherited or acquired).

• Acquired: Liver disease, vitamin K deficiency.

• Manifestations: Large bruises, hematomas, prolonged GI bleeding, urinary tract and joint bleeding.

Von Willebrand Disease

• Cause: Deficiency/defect of vWF (Von Willebrand Factor), affecting factor VIII-vWF complex.

• Manifestations:

  • Bleeding, excessive menstrual flow, prolonged bleeding time with normal platelet count.

  • Autosomal dominant inheritance.

• Avoid: Aspirin.

Hemophilia A

• Cause: X-linked recessive disorder, usually in males, with mutation in factor VIII gene.

• Manifestations:

  • Mild to moderate cases: bleeding from trauma/injury.

  • Severe cases: spontaneous bleeding in childhood, mostly in joints (hips, knees, elbows, ankles).

• Treatment: Injury prevention, factor VIII replacement, avoid ASA/NSAIDs.

Disseminated Intravascular Coagulation (DIC)

• Cause: Widespread coagulation and vascular compartment bleeding, usually due to trauma or disease process.

• Manifestations: Petechiae, purpura, puncture site leaks, severe hemorrhage, microemboli.

• Risk Factors: Cancer, pregnancy.

• Outcome: Can lead to multiple organ failure.

Blood Loss Anemia

• Cause: Acute or chronic blood loss.

• Acute: Leads to cardiovascular collapse, hypoxia.

• Chronic: Caused by GI bleeds, menstrual disorders, iron deficiency.

• Manifestations: Fatigue, weakness, pallor, tachycardia, dyspnea, angina.

Hemolytic Anemia (Sickle Cell Disease)

• Cause: Inherited Hemoglobin S mutation leading to deoxygenation-induced sickling.

• Manifestations:

  • Severe hemolytic anemia, chronic jaundice, vaso-occlusive crises.

  • Complications include acute chest syndrome, bone pain, spleen destruction.

  • Higher risk of infection.

• Triggers: Cold, stress, infection, physical exertion.

Thalassemias (Alpha and Beta)

• Cause: Disorders of hemoglobin synthesis.

• Alpha: Most common in Asian populations.

• Beta: Most common in Mediterranean populations.

• Manifestations: Anemia, splenomegaly, bone changes (osteoporosis), iron overload.

• Treatment: Regular blood transfusions, iron chelation therapy, stem cell transplant.

Iron Deficiency Anemia

• Cause: Dietary iron deficiency leading to compromised hemoglobin synthesis.

• Manifestations: Fatigue, palpitations, pica, smooth tongue, spoon-shaped nails.

• Treatment: Iron supplementation.

• B12 Deficiency Anemia

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  • Cause: Vitamin B12 deficiency due to dietary lack or absorption issues (e.g., proton pump inhibitors, GI diseases).

  • Manifestations: Similar to other anemias, neurological changes, difficulty making blood cells.

  • Treatment: B12 supplementation.

Folic Acid Deficiency Anemia

• Cause: Folic acid deficiency (due to malnutrition, pregnancy, neoplasms, alcohol use).

• Manifestations: Megaloblastic changes without neurological changes.

• Treatment: Folic acid supplementation.

Polycythemia

• Cause: Increase in RBC mass, which can be primary (polycythemia vera) or secondary (compensatory to hypoxia).

• Manifestations: Hypertension, headache, dizziness, plethoric appearance, thrombosis, pruritus, pain.

• Treatment: Phlebotomy (for polycythemia vera), treat underlying condition (for secondary).

Neutropenia

(normal = 1000 cells/uL). Less than 500 = neutropenic precautions (high infection risk).

• Infection-related: Most commonly viral, but bacterial and parasitic infections can also cause neutropenia.

• Drug-related: Common in anticancer drugs.

• Patient factors: Age, disease, nutritional status, bone marrow damage.

• Symptoms: Skin lesions, stomatitis, pharyngitis, diarrhea, fever.

Mononucleosis

Self-limiting infection, often caused by Epstein-Barr virus.

• Clinical course: Gradual onset, 4-6 weeks incubation, prodromal malaise, anorexia, chills.

• Symptoms: Fever, pharyngitis, lymphadenopathy, petechiae of the palate.

• Complications: Splenomegaly, hepatitis, myocarditis, encephalitis, airway obstruction, hemolytic anemia.

• Diagnosis: Monospot (heterophile antibodies) - false negatives in early stages.

Non-Hodgkin Lymphoma

• Clinical features: Dependent on cell type and stage.

• Common symptoms: Lymphadenopathy, fever, night sweats, weight loss, and hypogammaglobulinemia (decreased B cells).

• Diagnosis: Biopsy, imaging, and molecular markers.

• Treatment: Chemotherapy, radiation, stem cell transplant.

Hodgkin Lymphoma

• Clinical features: Painless lymphadenopathy, usually above the diaphragm, constitutional symptoms (fever, night sweats, pruritus).

• Progression: Late-stage involvement of liver, spleen, GI, CNS.

• Risk factors: Carcinogens, viruses, genetic factors.

• Treatment: Chemotherapy, radiation.

Leukemia

Malignant hematopoietic precursor cell disorder, causing the proliferation of abnormal white blood cells.

• Types: Acute (ALL, AML) and Chronic (CLL, CML).

• Etiology: Radiation, benzene, toxins, drugs, and some cancers.

• Symptoms: Fatigue, fever, night sweats, weight loss, bleeding, bone pain, infection.

• Diagnosis: Bone marrow biopsy, blood tests, genetic markers (e.g., Philadelphia chromosome).

Acute Lymphocytic Leukemia (ALL)

• Most common in children, involves pre-B and pre-T cells.

  • Symptoms: Sudden onset, fatigue, fever, night sweats, weight loss, bleeding, bone pain.

  • Diagnosis: Immature WBCs >60%, bone marrow crowding, anemia, thrombocytopenia.

  • Treatment: Induction, intensification, maintenance.

Acute Myelogenous Leukemia (AML)

• Acute Myelogenous Leukemia (AML)

• Back: Primarily in older adults, affects myeloid precursor cells, inhibits terminal differentiation.

  • Symptoms: Fatigue, fever, night sweats, weight loss, bleeding, bone pain, infection.

  • Diagnosis: High blast count, bone marrow suppression (anemia, thrombocytopenia).

  • Treatment: Chemotherapy, stem cell transplant.

Chronic Lymphocytic Leukemia (CLL)

Most common leukemia in older adults.

• Symptoms: Lymphadenopathy, fatigue, weight loss, hypogammaglobulinemia.

• Diagnosis: Isolated lymphocytosis (>20,000 uL).

• Treatment: Often observation for indolent cases, stem cell transplant for high-risk cases.

Chronic Myelogenous Leukemia (CML)

Proliferation of granulocytes, erythroid precursors, and megakaryocytes due to Philadelphia chromosome abnormality.

• Phases: Chronic, accelerated, and terminal blast crisis.

• Symptoms: Weakness, weight loss, leukocytosis, splenomegaly, constitutional symptoms in accelerated phase.

• Diagnosis: Philadelphia chromosome (translocation) in 90% of cases.

• Treatment: Tyrosine kinase inhibitors, stem cell transplant.