Patho 280 final review notes, Study Guides, Projects, Research of Pathophysiology

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1. Crohn's Disease •Inflammation and ulcerations occurring ANYWHERE in GI tract from mouth to anus - Patchy, "skip" lesions - Ulcerations may be full thickness •High risk of peritonitis and fistulae's
2. Ulcerative Colitis •Inflammation of Colon/Large Intestine ONLY
   • Continuous ulcerations beginning in rectum and moving upward
   • Ulcerations only involve the mucosa and submucosa (superficial)
   • Higher risk for colon cancer 3. Cirrhosis Patho- physioly
     • Hepatocytes get replaced with fibrotic and scarred tis- sue. Permanent and irreversible.
3. Liver Disease s/s Confusion/disorientation •Edema/Peripheral edema (low albumin)
   • Ascites (portal HTN) •Jaundice - yellowing of skin & eyes
   • Pruritis (itching) •Anemia (low HgB) •Bruising or bleeding easily (low platelets) •Bilirubinuria (dark colored urine)
   • Clay colored stools 5. Esophageal Varices

• Pathophysiolo gy
• Abnormal, enlarged veins in the esophagus. Usually due to a complication from cirrhosis.

• Complications - Ruptured • Upper GI bleed- hemateme- sis • Hypotension • Low HCT/HGB

6. GI Bleeds Signs/Symptoms: •Hematemesis: bright red blood, esophageal source •Coffee ground emesis: from stom- ach, darker in appearance

• Melena = black and tarry stools, usually indicative of up- per GI bleed black, tarry appearance caused by digestion process
• Causes: •Ruptured esophageal varices •Bleeding peptic ulcer
• Esophagitis or gastritis
• Cancer (Gastric or Esophageal) •Medications such as NSAIDS, ASA, steroids 7. Gallbladder dys- funtion Cholelithiasis no s/s, No duct blocked Biliary Colic: s/s Intermittent RUQ pain, N/V, resolves hours later. Duct blocked: Cystic duct (temporary) Cholecystitis (inflammation/ infection due to prolonged cystic duct blockage) S/s: RUQ pain, N/V, fever chills Duct blocked: Cystic duct (permanent) Gallstone Pancreatitis: S/S: Intense epigastric pain radi- ating to upper back and left shoulder, s/s of cholelithiasis Duct blocked: common bile duct pancreatic duct

8. gastritis Pathophysiology: Inflammation of the stomach lining. Causes/ Risk factors: Medications -> NSAIDS, aspiring, steroids ETOH consumption, smoking. NG Tubes Recurrent H.Pylori infection
9. GERD Pathophysiology: Reflux of acid from stomach into esoph- agus via the lower esophageal sphincter. Signs/Symptoms: Epigastric pain often worse at night (heartburn) Chronic cough Sour/bitter taste in the morning
10. Pancreatitis Pathophysiology: Auto-digestion of pancreas due to acti- vation of digestion enzymes within the pancreas. Cause: Men- alcoholism Woman- biliary disease Labs: Elevated amylase, Elevated lipase, hypocalcemia, elevated WBC

11. Small Bowel Small bowel malabsorption, can occur with a lack of di- gestive enzymes Small bowel obstructions: Usually, adhesion or strangu-

lated hernia Signs/symptoms: Central colicky intermittent pain, cramping. Frequent and severe vomiting Severe fluid imbalance and metabolic alkalosis (vomit- ing) Some passage of stool initially then obstipation Mils abdominal distention Complications: Bowel perforation Electrolyte imbalance

12. Large Bowel Large bowel obstructions Colon cancer or volvulus Sings/ symptoms: Crampy, lower abdominal pain Absolute constipation Minimal or no vomiting Massive abdominal distention Complications: Bowel perforation Electrolyte imbalance

13. Viral Hepatitis Hepatitis A: Transmission route: fecal/ Oral

Vaccine: Yes Cure: recovery from illness results in lifelong immunity Hepatitis B: Transmission route: Blood to blood and sexual contact Vaccine: Yes Cure: no cure (treatment available) Hepatitis C: Transmission route: Blood to blood Vaccine: No Curable (8-12 week treatment)

14. Appendicitis Patho: Inflammation of the appendix Sign/ Symptoms: Central abdominal pain that migrates to the RLQ Fever vomiting no appetites
15. Celiac disease Patho: Immune reaction to gluten leading to villi destruc- tion Diet Modification Avoidance of all foods containing gluten ( No wheat, rye, bran or barley) Can have corn and rice
16. Diverticulosis Presence of outpouchings within the colon. Asymptomatic, risk of inflammation -> diverticulitis

17. Diverticulitis Inflammation and infection of outpouchings within the colon, usually due to blockage s/s fever, nausea, leukocytosis (increased WBC) LLQ pain
18. Paralytic ileus Patho: Lack of peristalsis causing lack of forward motion of stool in intestines Usually after abdominal surgery or a serious illness (sep- sis, burns)
19. Peptic Ulcers Gastric Ulcers: Ulceration of the stomach/gastric lining. Pain WITH eating Duodenal Ulcers: Ulceration of the duodenum/ small in- testine Pain RELIEVED by eating.

20. Bacterial Testing

size/shape Cell wall staining-gram+(purple) and gram - (pink) Culture- find the specific bacterial infection growing from patient sample (i.e. blood, body fluids) Sensitivity test- determines which antibiotic will treat the bacterial infection

21. Septicemia Infection that results in sever inflammation, unstable vital signs (BP, HR) potentially Multi- organ failure Begins with systemic inflammatory response (SIRS) - 2 abnormal findings (see chart) SIRS plus an infection suspected or confirmed= sepsis Severe sepsis= sepsis+ signs of an organ damage+ hy- potension+ increasing lactate Septic shock 22. Renin-An- giotensin-Aldos- terone System **(RAAS)
22. Acute Kidney** In- jury Types of in- juries

Activated by: LOW blood volume (i.e, blood loss, fluid volume deficit) Low blood pressure (i.e, Hypotension) Net effect: I n c r e a s e d p l a s m a v o l u m e I n c r e ased blood pressure Increase vascular tone Increased cardiac output Pre-renal: Decreased renal blood flow- hemorrhage, de- hydration Intra-renal: Damage to renal architecture-drugs, disease.

Post-renal: Obstruction of urinary outflow system- BPH

24. Acute Kidney In- jury Phases **of Recovery

25. Chronic** Kidney **Disease
26. Nephrotic** Syn- drome Oliguric (<400ml of urine in 24 hours) Urinalysis: casts, RBC, WBC's, hyperkalemia/hyponatremia, elevated BUN and Creatinine. Fatigue and malaise Diuretic (excessive urine>2-4L per day) Gradual increase in urine output Hypovolemia, dehydration, hypotension. BUN/Creatinine levels still high Recovery (urine returns to normal 1-2 L per day) GFR improves BUN/creatinine return to normal Renal damage leads to reduced glomerular filtration re- sulting in excess fluid and waste accumulation within the body. Serum changed in CKD: Increases: sodium, potassium, chloride, hydrogen ions, magnesium, phosphate, BUN, Creatinine, PTH Decrease: calcium, erythropoietin, vitamin D, RBCs. Damage to the glomerulus (not inflammatory).

Protein loss is not stopped so most s/s are caused b hypoalbu- minemia S/S: Hypoalbuminemia-

decreased serum albumin,

EDEMA (periorbital, extremities) Hyperlipidemia-> hepatic compensation -> creation of more proteins, but also more FATS (** Hyperlipidemia) Proteinuria >3.5 g in 24 hours= foamy urine

27. Acute Glomerulonephri- tis (Nephritic **syndrome)

28. Urinary Inconti-** nence Glomerulonephritis -> INFLAMMATION of the glomeruli Cause: antigen-antibody complex causing inflammation of glomerulus and basement membrane -> leaky base- ment membrane (to ALL things) S/S: cola-colored urine, HTN Stress Incontinence: sphincter/ valve malfunction. Risk factors: Multiple pregnancies, female>male, age 40's Urge incontinence (OAB): detrusor muscle overactivity. Risk factors: sudden, frequent urges more common in females>males. Overflow incontinence: chronic bladder distension due to retention/obstruction.

Risk factors: BPH, incomplete emptying, Male>females. Neurogenic bladder: due to SCI, no sensation of fullness. Risk factor: Brain unable to sense fullness of bladder.

Functional Incontinence: Inability to hold urine due to underlying psychiatric or CNS causes. Risk factors: strokes, Alzheimer's. 29 . Lower Urinary Acute cystitis. Tract Infection Bladder infection (UTI) S/S: dysuria, frequency, urgency, cloudy or bloody urine. No systemic symptoms (no fever) 30 . Upper Urinary Acute pyelonephritis Tract Infection Bacteria reaches the kidney. (UTI) S/S: dysuria, frequency, urgency. "systemic symptoms" -> fever, flank pain, malaise, N/V. Urosepsis possible (bloodstream infection) Risk Factors: Diabetes, HIV/ immunodeficiencies, anatomical abnormalities. 31 . Endometriosis Growth of endometrial tissue outside the uterus. S/S: painful period (dysmenorrhea), pelvic pain/ cramp- ing, pain with bowel movements or urination, excessive bleeding, infertility.

32. Pelvic Inflamma- tory Disease 33.^ Testicular^ Tor-^ sion

Infection of the female reproductive orans including uterus, fallopian tubes, ovaries and cervix. Complications: Permanent damage, infertility. Twisting of the cord that supplies blood to the testicles (acute/emergent). Often occurs several hrs. after vigorous activity, minor injury or while sleeping. S/S: sudden onset of unilateral scrotal pain, scrotum swelling, abdominal pain, N/V, higher than normal testicle, frequent urination, fever.

34. Cryptorchidism (undescended testes) Testes remain in the abdomen or inguinal canal. Higher prevalence in premature born males. Complication-risk for infertility and testicular cancer. 35. BPH (benign pro- static hyperpla- sia) Hyperplasia of prostatic tissue that will cause compres- sion of urethra and urinary obstructions S/S- obstructed urine flow, difficulty urinating, drippling, increased frequency/urgency, nocturia, decreased flow strength. Risk factors: infection, post renal kidney injury.
35. Types of cancer Carcinomas - epithelial cell cancers (i.e., oral, skin, lung, colon, breast, prostate, uterus, etc.) • Sarcomas- connective tissue (i.e., osteosarcoma of bone
    • present with bone pain/fracture) • Lymphomas- lymphatic tissue (i.e., Hodgkin's/Non-Hodgkin's lymphoma) • Present with en- larged lymph nodes, fever, night sweats

Melanomas- pigmented cells (i.e., Malignant melanoma

• ABCDE of abnormal moles) •

37. Characteristics of Malignant **Neoplasms

38. Acute** Inflamma- tion Purpose Leukemias- WBC cancers • Present with fever, shortness of breath, bruising • Glioma's- Neural tissue - brain and spinal cord (i.e., Glioblastoma - present with neuro symptoms) Uncontrolled/disorganized growth of tissue, often occur from dysplastic cells Evades immunity of the body • Autonomy - grow uncontrollably & quickly Anaplasia - lack differentiation (poorly differentiated) Angiogenesis - produces its own blood vessels • Metastases - Spread of cancer cells from the primary site to other locations through the blood or lymph system • Common sites - lungs, liver, brain, bone Destroy : any offending agent or antigen Wall off & localize the area, Isolate site to limit damage, Clotting system - stop bleeding, Swelling will wall off the area Turn on the immune system • Release cytokines & other factors to turn on the Adaptive Immune System • Stimulate • Tissue healing through growth factors

• Angio- genesis - new blood vessels formed • Tissue regeneration
  • Scar formation

39. Histamine Local vasodilation Increase capillary permeability to improve the recruitment of leukocytes to the area

40. Innate Immuni- ty (non-specific defense mecha- nisms) Timeline 0-12 **hours

41. Adaptive Immu-** nity (specific de- fense mecha- nisms) Timeline **1-7 days
42. Antibodies or** Im- munoglobins 43. Rheumatoid Arthritis (RA)

1st Line of Defense: Skin M u c o u s M e m b r a n e s S e c r e t i o n s o f S k i n Secretions of mucous membranes. 2nd Line of Defense: Macrophages Other phagocytes(i.e. neutrophils, NK cells) Antimicrobial proteins The inflammatory response (e.g. redness, fever) 3rd Line of Defense: Lymphocytes (B & T cells) Antigen-specific Antibodies Memory IgG - circulates in body fluids, long-term immunity to a specific infection •Passed from mom to baby through placenta for protection •Lasts for years in the body as a memory to a specific infection

• IgA - found in secretions of mucus membranes, prevents antigens from entering the body (i.e., saliva, tears)
• IgM - circulates in body fluids, initial response to a spe- cific infection
• IgE - found on mast cells in tissue, present with inflamma- tion, allergies & parasites in the body •Causes mast cell release of histamine, leading to vasodilation & increase permeability - edema
• IgD - found on surface of B-cells, acts as an antigen receptor Chronic, progressive autoimmune disorder that attacks multiple areas of the body including the joints.