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3. GU and GI- Pathophysiology --Exam 3

Terms in this set (85)

Acute Diarrhea
-Frequent passage of loose or watery stools persisting 3-5 days that are not bloody, purulent, or greasy
-Acute is < 2 wks. duration
-Most cases are self-limited and brief, and require only symptomatic management

Large Volume:
-Viral or bacterial infection of large or distal small intestine
-Can alter volume and electrolyte balance

Small Volume:
Frequent loss of small amounts of stools
Characteristic of ulcerative colitis and Crohn's disease *Other Symptoms: Fever, Abdominal pain/discomfort, Headache, Malaise, Vomiting
Constipation
-Changes in the frequency, size, and consistency, and ease of stool passage.
-One of the more common and persistent presenting complaints
-Among the most frequent reasons for self-medication, especially in the elderly
-< 1 stool every 3 days
CAUSES: dehydration, delayed gastric motility, sedentary lifestyle, low fiber diet, psychogenic(belief), drugs side effects
TX: 1. lifestyle changes (^fiber, exercise, bowel train) 2. if no work... lax, softeners, enemas, suppository
Anorexia
Loss of appetite or desire for food

Occurs as a symptom of other GI problems

Also present with conditions not associated with the GI tract
Nausea
-Subjective, unpleasant sensation that may precede vomiting
-Caused by:
-->Distention or irritation anywhere in the GI tract
-->Stimulated by higher brain center
Vomiting****
1. Complex reflex mediated by vomiting center in the medulla oblongata of the brain
2. Occur in response to:
-Excessive distention or irritation of the stomach or duodenum
-Chemical stimulation
-Pain
3. Projectile vomiting occurs with direct stimulation of vomiting center—due to increase ICP(sign of anneurism/bleed or other issues)
4. Symptoms that precede vomiting
-Nausea
-Tachycardia
-sweating

****Pain that pain is the body's primitive reflex that causes the body to get rid of toxins (vomit).
Types of Abdominal Pain***
1. Parietal Pain
caused by stimulation of pain receptors in the parietal peritoneum or abdominal wall. The pain is localized, sharp, intense, and one-sided (lateralized). LOCALIZED

2. ***Visceral Pain
caused by stimulation of abdominal organs; pain is vague, diffuse (nonlocalized), and dull .***NON LOCALIZED

3. Referred Pain
is felt at a distance from the affected tissue or organ; is localized at some point along the afferent nerve pathway of the organ or tissue
Intestinal Obstruction***
1. Impaired movement of intestinal contents
2. Mechanical obstruction
-***Caused by any condition that affects the patency of the bowel lumen
-Tumor
-Adhesion
-Severe constipation
3. Can lead to abd distention, and alteration of F&E
4. In severe cases can lead to ischemia of bowel, acidosis, perforation, shock, sepsis, and death

S/S: pain-in waves coming with peristalsis, distension(PROXIMAL to obstruction), nausea/vom, anorexia, diarrhea if not complete obstruction, decr. bowel sounds- or absent upon perforation BUT leads to systemic infections due to leaking contents, (borborygmus-(high pitch/hyperactive sounds)), ab tender, rigidity, fever/shock(after systemic/perforation)

LLEUS: block of large/small intestine b/c perisalis stops (48-72 hrs mostly)
-Caused by: ab surgery, reduced blood supply to ab, meds
-S/S: ab cramp, distention, nausea/vom, fail pass gas or stool
***Ileus: Occurs due to lack of peristalsis BUT it is NOT mechanical it is the cessation of peristalsis. Usually self limiting and temporary. Main cause is abdominal surgery (after anesthetic paralysis from general anesthesia) Could also be due to the "cutting into" of the abdomen
Acute Abdomen
-Defined as an episode of severe abdominal pain that lasts several hours or longer and requires medical attention.
-The acute abdomen usually, but not necessarily, has a surgical cause.
-The key feature in the evaluation of patients with acute abdomen is early diagnosis.
-Common gyn causes
lower quadrant pain: pelvic inflammatory disease (PID), fibroids, ovarian cyst
-Medical causes:
lower lobe pneumonia, acute MI, diabetic ketoacidosis, acute hepatitis.
-Appendicitis
triad of RLQ pain, anorexia, and leukocytosis is the most sensitive diagnosis tool.
Peritonitis
Inflammation of the Peritoneum
Causes: Follows perforation of gut or organ into peritoneal cavity, Perf. Ulcer, Ruptured appendix, Perf. Diverticulum, PID

The perforation and release of pressure will actually cause more pain (pt will show guarding)

S/S: Pain Especially over inflamed area, May be rebound in nature, Nausea and vomiting,--> Rigid abdomen(med emergency), Tachycardia/shock, Fever, Increased WBC from all bacteria perforated into the gut cavity
Peptic Ulcer Disease***
1. Ulceration of the Upper GI mucosa exposed to acid-pepsin secretions when there is an imbalance between gastric protective mechanism and irritating factors.
-->Normal stomach ph is about 2, which kills many swallowed bacteria and virus
-->Acid production increases after a meal and consequently, symptoms associated with gastritis and gastric ulcer often improve with eating/antacid use
**CAUSES: Gastric Irritation(**h. pylori, excessive NSAIDS, zollinger-ellision, stress ulcer)
RISK FACTORS: advanced age, warfarin, NSAIDS, coricosterioids, smoking
Helicobacter pylori
-Bacteria capable of growing, even flourishing, in the low pH (acidic) environment of the stomach and proximal duodenum
-A gram-negative rod with flagella that propel it through the protective mucus layer to access the underlying tissues
-Cofactor of some gastric cancers and a cause of some types of chronic gastritis and most peptic ulcers
Pepic Ulcer Disease Patho****
1. Excessive acid
-Leads to break or ulceration in the mucosa of the stomach or duodenum
-Breaks allow the mucosa to be subjected to an acid or alkaline environment
-Autodigestion occurs
2. Decreased mucus production
-Leaves mucosal cells unprotected from acid environment
3. Increased delivery of acid
-Too rapid movement of stomach contents and acid into the duodenum can overwhelm protective layer of mucus
PUD:
Duodenal ulcer vs Gastric ulcer
*Duodenal ulcer (DU):
--4 times more common than GU
-- 25-75 yrs.
--Epigastric burning 2-3 hrs PC; relief with foods or antacids
--Awakening at 1-2 am with symptoms are common, Otherwise has periods of feeling well

*Gastric ulcer
--More common among NSAID users
--55-65 yrs. (rare prior to age 40)
--Pain often reported with or immediately after meals
--N/V, weight loss is common
PUD Clinical Manifestations
PUD Manifestations
-Dyspepsia
-Pain when stomach is empty (duodenal)
-Pain immediately after or during eating (gastric)
-Weight loss (gastric)—weight gain (duodenal)
-Hematemesis
-Melena
-In severe cases can lead to perforation and hemorrhage
PUD:
Diagnosis and Treatment
Diagnosis:Endoscopy, Blood test
Presence of antibodies to H. pylori, CBC—decrease RBC, HCT, Hgb, Upper GI barium studies, Stool specimen—occult blood

Treatment: Avoid foods that cause excessive acid secretion, Avoid alcohol and caffeine
Discontinue or reduce NSAIDs, Stop smoking, Reduce stress, Medications(Antacids, Antihistamines, Antibiotics)
GERD***
-Reflux of gastroduodenal contents into the esophagus with or without esophageal inflammation
-->Incompetent lower esophageal sphincter (LES)
--> Esophageal mucosal irritation from HCL acid and pepsin
-->Delayed esophageal peristalsis
-->Delayed gastric emptying
CAUSES: LES relaxations (narcotics, ca ch blockers, etoh, nicotine, chocolate, peppermint
S/S: heartburn, regurg of food, burning after eating, chest heavy, pressure radiationg neck/jaw/shoulders, laryngitis, barret esophagus, **GASTRIC CANCER
TEST: barium radiograph of upper GI, endoscopy(more accurate)
TX: wt decr.(obese), elevate head of bed, avoid large meals and carbonation3hr before bed, avoid stoop/bend/tight clothes, drugs LES tone
Hiatal Hernia***
-is a condition in which the stomach protrudes through the diaphragm-Can herniate to thorax
-can be asymptomatic or may cause symptoms of gastroesophageal reflux
-Diagnosis is made by barium swallow or endoscopy
-Treatment is the same as for GERD
-->May need surgical repair if very large
***If the pouch of the stomach becomes ischemic it can actually cause lack of flow leads to death to tissue of that part of the stomach
Diverticulitis***
-Inflammation of one or more diverticula in the bowel wall with microperforation and abscess formation in the pericolic fat.
-Diverticulosis - herniation of mucosa through the muscular wall of the colon; found most often in the sigmoid colon but may occur anywhere in the GI tract
-Higher in individuals with low fiber diet
CAUSES: not clear (more common >60yrs)
S/S: **ab pain usually in LLQ, altered bowel, pain w/defecate, LOW GRADE FEVER, nausea/vom, pos guiac
TEST: CBC slight leukocytosis, incr sed rate, normal urine(unless rectal fistuals), abdominal filums obstruction, barium enema for confirmation and r/o
Treatment: diverticulitis: antibiotics, rest, fluids. diverticula tx: prevent constipation with incr water, diet changes
Appendicitis
**KNOW classic signs/sympt
-Inflammation of the vermiform appendix
-Obstruction of the appendix with fecalith, stricture, foreign body or neoplasm
-Occurs in all age groups, but more common in males between 10 and 30 years old
-One of the leading causes for abdominal surgery
S/S: PAIN RLQ, *ANOREXIA and N/V, max tender at "mcbuney's point", RLQ rebound tender, Rovsing's sign (RLQ pain w/palpation of LLQ), Psoas sign (pain with right thigh extension), Obturator sign (pain with internal rotation of flexed right thigh)
PERFORATION AFTER 24HRS: abdominal rigidity, ab tender, high fever, decr bowel sound, vom, shock
IBS
MOST COMMON DX amoung GI PRACTICE (mostly females)
-IBS is defined as a functional bowel disorder in which abdominal pain is associated with defecation or a change in bowel habits, with features of disordered defecation and distention.

Rome II Diagnostic Criteria for Irritable Bowel Syndrome (IBS)
At least 12 weeks, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that has 2 of 3 features:
Relieved with defecation
Onset associated with a change in frequency of stool
Onset associated with a change in form (appearance) of stool
S/S: Abnormal stool frequency (for research purposes, "abnormal" may be defined as greater than three bowel movements per day and less than three bowel movements per week) , Abnormal stool form (lumpy/hard or loose/watery stool) , Abnormal stool passage (straining, urgency, or feeling of incomplete evacuation) , Passage of mucus
Bloating or feeling of abdominal distension
IBS Treatment:
Most pts. with IBS have only mild symptoms and little disability
Decrease stress
Warmth to abdomen
Dietary changes
increase fiber bran &/or bulk laxatives
avoid the obvious foods that cause abdominal distress
Ulcerative Colitis
-is a chronic inflammatory disease of the colon manifested by diffuse ulceration of the colonic mucosa, especially the rectum and sigmoid colon
-Familial
-Most often presents in early adulthood
-Autoimmunity leads to inflammatory ulceration in the large intestine with mucosal erythema, edema, and friability.
-Mucosal ulceration and edema lead to narrowing of the colonic lumen, diarrhea, and significant bleeding (hematochezia).
-Ulcerative colitis begins in the rectum and advances up through the colon in a continuous manner and does not "skip" parts of the mucosa.
-10 to 20 stools per day
-crampy abdominal pain and dehydration
-Bleeding can be significant and can cause anemia
although life threatening, hemorrhage is uncommon
-Chronic inflammation is a risk for colon cancer and leads to an increased risk of infection, perforation, and strictures
-Diagnosis is made by colonoscopy. Management includes antiinflammatory medications , Hospitalization and colonic resection with colostomy placement may be necessary
Crohn's Disease
-A chronic inflammatory disease of the bowel characterized by patchy inflammation of all layers of the GI tract - submucosal layer and ileum and colon
-Incidence
young adults and teenagers,
Familial
-Develops slowly with remissions and exacerbations
-Stress may trigger exacerbations
CAUSES: unknown-- autoimmune, theories--infection, allergy, psychosomatic dietary.....
Crohn's Manifestations***
-Nausea and vomiting
-Flatulence
-Colicky pain - right lower quadrant, increasing as disease progresses
-Malabsorption ****
Stools: 3-5 semisolid foul-smelling stools/day, Mucus in stools with possible pus, Intermittent, usually nonbloody diarrhea, Urgency to defecate at night)
-Weight loss caused by anorexia
-Fluid and electrolyte imbalance
-Malaise
-Low-grade fever
-Elevated WBC
-Iron-deficiency anemia***
-Perianal abscesses and fistulas
-hypoalbuminemia
Crohn's Diagnosis and Treatment
Diagnosis:
-CBC(Increased WBC, Decreased RBC, Hgb, Hct)
-Barium enema/Sigmoidoscopy/CT Scan
-High ESR
-Electrolyte abnormalities

Treatment:
-Nutritional supplements and diet education (low residue, high-protein, high-calorie)
-Psychological support - stress management
-Total parental nutrition
-Medications(Anti-inflammatory drugs, Antibiotics, Vitamin, mineral and electrolyte replacements)
Cholecystitis
-Inflammation of the gallbladder occurring acutely or chronically, often secondary to previously asymptomatic gallstones
-About 90% related to presence of bile (30%) or cholesterol (70%) calculi
-Diameter from 1 mm to 4 cm
-When a stone becomes impacted in the cystic duct, inflammation develops behind the obstruction
Cholecystitis: Causes:
If not relieved pressure builds in gallbladder and leads to disten., ischemia, gangrene, perforation w/subsequent abcess formation and less freq generalized peritonitis
*CAUSES: Advanced age, female, and being obese are all risk factors, gall bladder sludge, bacteria, stricture, neoplasms
Acute Cholecystitis Signs/Symptoms
S/S: abdominal pain: sudden onset, intense, in epigastrium or RUQ, radiates to back or shoulder, Classic presentation is "biliary colic" a pain that starts out from mild (2-3 mins) steadily increasing in intensity and is present for 20 mins.+
N/V (75%), Recurrent attacks following meals (fatty) from 1-6 hrs. later
Local tenderness in epigastric and RUQ areas, Positive Murphy's sign - tenderness on palpating RUQ clinical findings are present only during an acute attack
2. Common Duct Stone: Jaundice, fever/chills, mild/marked hepatomegaly
3. Chronic cholecystitis: often asymptomatic, 20% symptomatic over 15-20yrs, mild dyspepsia following fatty meal
Cholecystisis
-Tests/Dx
-Treatment/Tx
Diagnosis: CBC - leukocytosis 12,000-15,000, ECG - to r/o MI
Liver function tests may be transiently elevated:AST, formerly termed SGOT, and ALT, formerly SGPT, slightly elevated along with elevation of alkaline phosphatase and serum amylase, Bilirubin mildly increased, Chest x-ray to r/o pneumonia, Ultrasound (US) of gallbladder may show stones, thickened gallbladder wall, Flat plate of the abdomen is not very useful since only 20-30% of all gallstones are radiopaque, NM GB Scan

TX: Elective cholesystectomy recommended for:
symptomatic pts. with radiologic or US evidence gallbladder disease
those at high risk for complications such as those with calcified gall bladder, gallstones > 2cm in diameter and diabetics
Conservative treatment for those who are asymptomatic:
only 30% of pts. who present with an acute attack will have a recurrence
avoid foods that seem to precipitate symptoms, otherwise no need to alter diet or restrict fats
treat dyspeptic symptoms with antacids (25-50% of pts. will respond)
Viral Hepatitis
The presentation of viral hepatitis, regardless of the agent, usually includes:
malaise, myalgia, fatigue, nausea, anorexia, aversion to cigarette smoking is often reported, mild fever is occasionally found, occasionally, arthritis-like symptoms and skin rash are also noted
Hepatitis A
1. Hepatitis A infection is caused by HAV (hepatitis A virus)
--Fecal-contaminated drinking water and food: Raw shellfish grown in contaminated water, fresh fruits and vegetables cleaned with contaminated water or fertilized with human waste
--hepatitis A is typically a self-limiting infection with a very low mortality rate - acute infection only, no chronic hepatitis or chronic carrier states
2. Prevent infection through food and water safety, immunization, and postexposure immune globulin use
3. Hepatitis A vaccine, which contains dead virus, consists of 2 injections 6 mos. apart
--consider providing vaccine to patients who reside or travel to areas where disease is endemic; food handlers; day care and long-term care workers.
Serum Markers of Hepatitis A
DON"T NEED TO KNOW THESE
1. Anti-hepatitis A virus IgM (anti-HAV IgM or HAV IgM)
-appears early in infection
-marker of acute hepatitis A infection
-disappears within 3-6 months
2. Anti-hepatitis A virus IgG (anti-HAV)
-appears approximately 1-2 mos after exposure to HAV
-in absence of anti-HAV IgM, marks immunity to HAV through prior infection or vaccine
-persists for years
Hepatitis B
1. The virus is transmitted through exchange of body fluids
--sexual contact
--IVDU with needle sharing
--occupational exposure in health care workers
2. Acute infection is usually symptomatic and mild to life threatening
3. Prevent with universal precautions, clean needle exchange, immunizations, safe sex.
4. Vaccine: recombinant hepatitis B vaccine, which does not contain live virus, is well tolerated

PhyExam FINDINGS: hepatomegaly with usually mild RUQ tenderness without rebound is found in about 50% splenomegaly in about 15%, Jaundice is not found in most cases
The course of the illness is typically 2 - 3 weeks, during this period, a gradual increase in energy, appetite and well-being is reported. Chonic HepB leads to liver cancer
Serum Markers of Hepatitis B
DO NOT NEED TO KNOW THESE
1. HBV surface antigen (anti-HBsAg)
-1St marker of infection
-may be present before increase in level of hepatic enzymes
-remains throughout course of acute and chronic HBV
->6 mos after acute infection indicates chronic hepatitisB
2. HB surface body (anti-HBsAb)
-Appears shortly after clearance of HbsAg
-90-95% develop HBsAb
-Implies clearance of HBV and recovery from infection
-With immunization, is usually present in measureable levels
- infection is not possible
3. Anti-HBc (IgM anti-HBc)
Found early in HBV infection when HBsAg present, Persists for 3-6 mos or greater
4. HBeAg (hepatitis Be antigen)
Found in early in HBV infection when HBsAg present, found during period or viral replication and greatest risk of infectivity
, persists for >3 mos after onset of acute infection, increased likelihood of chronic hepatitis B
Hepatitis C
1. Transmitted through the exchange of blood and body fluids
>50% of cases of HCV are caused by IVDU with needle sharing.
sexual transmission is low
maternal-fetal transmission is also uncommon and is usually limited to women with high circulating HCV levels.
2. The most frequent cause of blood transfusion-associated hepatitis, only 4% of all cases of HCV can be attributed to this cause
risk of transfusion: 0.1%
3. Incubation period is about 6-7 weeks
the infection rarely causes a serious acute illness.
DX: presence of anti-HCV
an antibody that persists in the presence of the virus and is not protective
Hepatitis D
1. HDV can only occur concurrently in the presence of HBV, it is only found in those with acute or chronic HBV.
2. A patient with HBV and HDV acute co-infection has a course of illness similar to a patient with HBV only.
If a patient with chronic HBV becomes superinfected with HDV, a fulminant or severe chronic hepatitis often results.
Cirrhosis
1. Liver tissue replaced by fibrous tissue
-ETOH
-Viral Hepatitis
-Biliary Disease
2. Scarring of channels disrupts flow into liver, leading to portal HTN and further liver failure***

MANIFESTATIONS: weight loss(b/c cannot absorb nutrient), acites(b/c not able to absorb protein), hepatomegaly(liver inflammed/scarred), jaundice(high level of biliruben), ab pain
COMPLICATIONS: portal hypertension, acites, spelenomegaly, liver failure (endocrine disorders, GI bleed, hepatorenal syndrome, hepatic encepthalopathy

DX: Liver Funct Test(ALT/AST/ALK Phos/Bilirubin), Coag studies, CBC, CT abdomen, Ammonia levels, Fluid and Electrolyte imbalance
TX: address underlying cause, TIPS, Paracentesis, diuretics, lactoulose, prevent infection, liver transplantion
****Cholelitheasis vs Cholecystitis
Choleleteasis: just the presence of gallbladder stones
Cholecystitis: if a gallbladder stone impact the flow, they cause inflammation of the gallbladder. (hallmark sign is pain that radiates to shoulder)
Acute Pancreatitis
Activated pancreatic enzymes auto-digest pancreas
***CAUSES: #1 cause is gall stones in common duct, Alcohol abuse, Hyperlipidemia, Hyperparathyroidism, Infections, Surgery/Trauma, Drugs

CLINICAL MANIFESTATIONS: May follow heavy meal/ETOH use
Severe epigastric pain radiating to back
ARDS
Tachycardia, hypotension, fever, Increased serum amylase/lipase, Decreased calcium, CT abd
TX: Rest pancrease/pain relief/IV fluids
****Causes of Different Hepatitis:
Hep A
Hep B
Hep C
HepD
HepA: Fecal contaminated water, liquid, foods. Sometimes a restaurant where someone does not wash hands after using bathroom. Possible foods: Raw shellfish grown in contaminated water, fresh fruits and vegetables cleaned with contaminated water or fertilized with human waste SELF LIMITING infection (low mortality) No changes in liver.
HepB: Sexual contact, IV drug use/needle, needle stick injury in health care. Carried in saliva, semen, and blood. Easily transmittable.
HepC: Exchange of bodily fluids and mostly by blood. IV drug use, materal fetal, blood transfusion (#2 cause of liver transplant)
HepD: only in prevence of HepB, it is a coinfection,
***Increased Portal Hyptertsion
high pressures in the portal vein due to Scarring of channels disrupts flow into liver, leading to portal HTN and further liver failure

Happens with Cirrhosis
GU SYSTEM NOTES
...
Renal Blood Flow
Kidneys receive 20% of cardiac output during rest; reduced to 2% to 4% during physical or emotional response

Abdominal aorta gives rise to renal arteries, which enter the hilum of each kidney; eventually branch into afferent arterioles, which enter glomerular capillary beds
Efferent arterioles leave the glomerular capillary bed; eventually converge into progressively large veins until leaving the kidney
Nephron Picture
1- Glomerular capsule
2- Glomerulus
3- Afferent arteriole
4- Efferent arteriole
5- Proximal Convoluted Tubule
6- Distal Convoluted Tubule
7- Collecting Duct
8- Loop of Henle
9- Peritubular Capillary
Function of Kidneys
-Primary role is to maintain body fluid volume and composition and to filter waste products for elimination
-Help to regulate blood pressure
-Participate in acid-base balance
-Produce erythropoietin for red blood cell (RBC) synthesis
-Metabolize vitamin D to an active form
Hormone endocrine Role of Kidney***
Renin
Release stimulate release of angiotensiogen → angiotensin I →
Angiotensin II
Increases BP - potent vasoconstrictor
Stimulates adrenal cortex to secrete:
Aldosterone

ADH Acts directly on renal tubular cells (collecting duct and distal convoluted tubule) making them more permeable to water
When present at certain level in blood, makes kidneys conserve body water
When absent or diminished in blood, kidney loses body water
Urine Formation
1. Glomerular Filtration
2. Tubular Reabsorption & Secretion
--Loop of Henle
--Distal/Collecting Tubules
--Regulation of Urine Concentration
Urine Production Rate
Adult: > 1 ml/min
Infants: > 0.5 ml/kg/hr
Children: > 1 ml/kg/hr
Oliguria: diminished urine output, less than minimal expected production rate
Anuria: no urine output
Ureters
-Location: behind the parietal peritoneum
-Structure: ureter expands as it enters the kidney to form the renal pelvis; subdivided into calyces, each of which contains renal papillae
-Functions: collect urine secreted by the kidney cells and propel it to the bladder by peristaltic waves
Urinary Bladder
-Location: behind symphysis pubis, below parietal peritoneum
-Structure: collapsible bag of smooth muscle lined with mucosa arranged in rugae, three openings- two from ureters and one into urethra
-Function: reservoir for urine until sufficient amount accumulated for elimination and expulsion of urine from body by way of urethra
Urethra
Female: behind the symphysis pubis, anterior to the vagina
Male: extends through the prostate gland, fibrous sheet, and penis
Structure: musculomembraneous tube lined with mucosa; opening to exterior called urinary meatus
Female: passageway for expulsion of urine
Male: expulsion of both urine and semen
***Glomerulonephritis
-Inflammation of the glomerulus
-Can be acute or chronic
-Acute glomerulonephritis is glomerular inflammation that is typically caused by group A poststreptococcal infection
-Chronic glomerulonephritis is a combination of several glomerular diseases that ultimately lead to chronic renal failure

**Can be due to --> Diabetes, htn, infection, lupus
Throat infection can precede glomerulonephritis
Chronic -->leads to renal failure --> damage lack of flow to the nephron (atrophy) -->decrease nephron function
Disorders of the Glomerular Function
-glucose or protein are abnormalities
1. Nephritic syndromes
-->Proliferative inflammatory response
2. Nephrotic syndrome
-->Increased permeability of glomerulus
3. Mixed nephritic and nephrotic responses
4. Chronic glomerulonephritis
5. Glomerular lesions associated with systemic disease

**Inflammation can lead to glomerular damage
Damage leads to protein in urine --> low protein on board (hypoproteinemia)
If chronic --> Hyperlipidemia -->liver tries to release more lipids to compensate
Types of Glomerulonephritis
-Acute Glomerulonephritis
-Rapidly Progressive Glomerulonephritis (RPGN)
-Chronic Glomerulonephritis

Chronic is more diabetes, htn, lupus
Glomerulonephritis: Clinical Manifestations***
-Proteinuria (varying degrees based on the specific disease)
-Flank or back pain
-Hematuria
-Decreased urine output Edema
-General signs of inflammation: malaise, fatigue, headache, anorexia, and nausea
-HTN
Glomerulonephritis Assessment
-History of recent upper respiratory or skin infection, or invasive procedures
-Blood pressure for baseline
-Urine for Blood, protein
-Presence of dyspnea, edema, neck vein engorgement

Therapeutic Interventions: Antibiotics such as penicillin to treat underlying infection
Dietary restriction of sodium, fluids, and protein based on clinical status
Diuretics and antihypertensive to control blood pressure, Rest; regular activity when hematuria and proteinuria resolve
Nephrotic Syndrome
Evaluation
-24-hour urine collection: protein >3.5 grams
-Serum albumin <3 g/dl
-Fat droplets in urine
-Increase in serum cholesterol, phospholipids, and triglycerides
-Confirmation by renal biopsy
TX: Focuses on treating the underlying problem, Diet and drug therapies,
Increase protein, Salt is restricted as is fat intake, Meds(hypolipodemic drugs- statins, steroid therapy and immune suppressants)
UTI
Urinary Tract Infections
1. Bacteria usually enter through the urethra
2. Host defenses include:
-->Washout phenomenon
-->Protective mucus
-->Local immune responses and IgA
-->Normal bacterial flora

RISK FACTORS: Age extremes
Sexually active women, Patients with:
An indwelling catheter Lower urinary tract obstruction (long time), Diabetes mellitus
Immunosuppression, Women(b/c short urethra)
UTI Pathogenesis***
*Escherichia coli (about 80% of uncomplicated and 20% of complicated cases)
-Klebsiella, Proteus
-Pseudomonas, Staphylococcus saporphyticus
-Candida (most common fungal)
-Schistosomiasis (most common parasitic)
UTI Cystitis
-Is an inflammation of the bladder wall usually caused by an ascending bacterial infection (E. coli most common)
-More common in females due to: shorter urethra, childbirth, anatomic proximity of the urethra to the rectum
-Occur in men secondary to epididymitis, prostatitis, renal calculi
UTI Urethritis
-Is an inflammation of the urethra caused by staphylococci, E. coli, pseudomonas species, and streptococci
-->Although inflammatory symptoms are similar to gonorrheal urethritis, sexual contact is not the cause
-->May cause prostatitis and epidymitis
UTI Urosepsis
Is caused by gram-negative bacteria
May result from an indwelling urinary catheter or an untreated urinary tract infection
-->Harder to treat (cell wall of gram negative stay around longer)
UTI Clinical Findings***
**Subjective --> Signs of cystitis --> NOT fever
*Subjective:
-->Urgency; frequency; pain and bearing down on urination
*Objective:
Nocturia; hematuria; pyuria; bacterial growth evident in urine culture
UTI Treatment
-Identification of causative organism through urine culture
-Pharmacologic therapy with antibiotics, urinary antiseptics, antispasmotics
-Diet directed toward altering the properties of urine (cranberry juice)
-Additional fluids to dilute the urine
-Warm sitz baths to provide comfort

**Can use cranberry juice to prevent UTI if feeling it coming on prevents adhesion of bacteria not used when already infected
Pyelonephritis
-It is either the presence of active organisms in the kidney or the effects of kidney infections
-Acute: is the active bacterial infection
-Chronic: results from repeated or continued upper urinary tract infections or the effects of such infections. Usually occurs with an anatomic urinary tract anomaly, obstruction, or vesicoureteral urine reflux
-Differs from a simple UTI in that the infection in pyelonephritis occurs proximal to the bladder in the ureters, renal pelvis, and renal parenchyma
***Upper: effecting ureters and all the way to the kidney itself. More complicated
DX: U/A: (urinalysis)shows a positive leukocyte esterase and nitrates; occasional RBCs, WBC casts, and proteinuria may be present Urine culture, Blood cultureIVP(IV pylogram injectable dye)
TX: Antibiotic to treat the infection
Fluid intake is recommended at 2 to 3L/day unless another condition requires fluid restriction, Pain medication, Diet with adequate calories and all food groups
Urinary Tract Obstruction
-can lead to renal failure
-can be caused by:
-renal calculi(kidney stones)
-a neurogenic bladder(cns cannot empty bladder)
-cancerous tumors
-obstructive uropathy (urine back up to kidney)
-demands urgent attention and intervention
*any obstruction from urethra to pelvis
Obstructive Uropathy
-A number of disorders can interfere with the flow of the urine at any point in the renal system
FACTORS: The location of the lesion.
Whether one or both of the upper urinary tracts are involved, The severity of the obstruction, The length of time that the obstruction has been present, The nature of the obstruction.
Hydroureter
Hydronephrosis
Ureterohydronephrosis
*Anything too large will eventually rupture
-Hydroureter - abnormal enlargement of the ureter.
-Hydronephrosis - abnormal enlargement of the kidney.
-Ureterohydronephrosis - abnormal enlargement of the ureter and kidney
Upper Urinary Tract Obstruction CAUSES
Variety of causes
-congenital abnormalities
inflammation
-tumors
-metabolic conditions(Diabetes)
*Most Common
KIDNEY STONES (crystalization)
Pathophysiology- Calculi
-Urine becomes concentrated with insoluble materials
-Crystals form from these materials and then consolidate, forming calculi
-Calculi remain in the renal pelvis and damage or destroy kidney tissue or they may enter the ureter
-Large calculi in the kidneys may cause tissue damage
-If obstruct urine flow may cause hydronephrosis
***RISK Factors for Renal Calculi
1. Age 20-40 years
2. Gender Men > Women (men: up to 20%, women: 5-10%)
3. Fluid intake- Persons who do not consume adequate fluids (dehydrated)
4. ****Diet- Excessive vitamin D and calcium ingestion, vitamin A deficiency
5. Lack of Exercise-based on underlying pathology: such as gout, Uti, Inflammatory bowel
6. Geographic location-Based on temperature, humidity, and rainfall. Living in the "sunbelt" of the U.S. increases risk of kidney stones because persons tend to become dehydrated
Types of Renal Calcui***
Calcium stones (i.e., oxalate or phosphate)
Magnesium ammonium phosphate stones
Uric acid stones
Cystine stones
***Calcium stones are most common type -->Lack of exercise allows calcium to come out of the bones (weak bones with more calcium in blood)

All are based on diet
Mg Ammon : UTI cause there
Uric acid : gout
Cystine :very rare with amino acid accumulation --> do not focus on this
Calcui****
Masses of crystals composed of minerals that are normally excreted in the urine
May form anywhere in urinary tract
Usually develop in renal pelvis or calices

***CAUSES: Dehydration,Infection, Changes in urine pH, Obstruction, Immobilization, Diet, Metabolic factors

*MANIFESTATIONS: hallmark is dull, aching flank pain that wraps around the lower back to the sides then pubic and genitals(may travel from lower back to sides and then pubic region and genitalia), Intensity fluctuates and can be excruciating, Nausea/vomiting, Hematuria, Abdominal distention, Oliguria

DX: KUB(kidney ureter bladder xray), Kidney ultrasound, urinalysis(show type of stone), 24hr collection, blood test

TX: Most pass naturally by vigorous hydration>3L/day, drug therapy(antimicrobials, analgesics, antiemetics), **Removing Calculi: Lithotripsy: shatter calculi into fragments for natural passing(shock waves to determine where it is, then pressure to break up and pass--ONLY FOR LARGE STONES, Cytoscope: surgical removal from utreter
Prevent by adequate fluid intake, restriction of vitC/vitD/Calcium
Lower Urinary Tract Obstruction (partial)
STDs can cause scarring
-several types , may involve the bladder, bladder neck, prostate, or urethra , symptoms are related to alterations in urine excretion

MANIFESTATIONS: Daytime voiding frequency , Nocturia, Poor force of urinary stream , Intermittency of urinary stream
Bothersome urinary urgency, sometimes with hesitancy , Incomplete bladder emptying

TX: may occur in either the kidney or bladder, Renal tumors may be small, benign tumors that are difficult to detect, or they may be larger malignant tumors that usually arise from the proximal tubule epithelial cells , Bladder tumors are fairly common; they are the fifth most common malignancy
Renal Cell Carcinoma***
1. Most common renal neoplasm (85%)
2. *Risk factors for development of RCC include tobacco use, obesity, and long-term analgesic use (not asprin)
3. Clinical Manifestations: Hematuria-blood in urine (most common) , Flank pain-but can be painless, Palpable flank mass, Weight loss
4. DX: Ultrasonography, Intravenous pyelography (IVP), CT scan or MRI , Renal angiography
Bladder Tumors
Evaluation is made through cystoscopic exam with tissue biopsy
Other evaluative tests may include urinalysis to rule out infection, urine cytology, transurethral biopsy, and X-ray examination

TX: depends on the size and type of cancerous lesion
may include transurethral resection or laser ablation, or in severe cases, radical cystectomy with urinary diversion and adjuvant chemotherapy for locally invasive tumors
Classification of Renal Failure
-Renal insufficiency: occurs when renal function is impaired to 25% the normal function
-Renal failure is classified into acute and chronic.
-->Acute renal failure is further classified into prerenal, intrarenal, and postrenal
Acute Renal Failure
-The sudden inability of the kidneys to regulate fluid and electrolyte balance and to remove toxic products from blood
-Usually follows trauma to the kidneys or overwhelming physiologic stress (e.g. burns, septicemia, nephrotoxic drugs and chemicals, severe shock, etc) that decreases blood flow to the glomeruli or to the nephrons
-Sudden and almost complete loss of glomerular and/or tubular function
Pre-Renal Failure
Most Common (acute renal failure)
Fix the volume (flow) and it will correct

Any condition leading to inadequate kidney perfusion (less than 25% of CO)
Reversible with reestablishment of adequate flow
***CAUSES: Easiest and most common is hypovolemia it is an easily reversible cause , Peripheral vasodilation leads to septic shock state. Note: If it is before the kidney it is called pre-renal
-->Other causes: Cardio-vascular disorders, Cardiac tamponade (pump not working), Heart failure/Myocardial infarction, *Hypovolemia/Hemmorhage, Burns, Dehydration, Diuretic overuse, Trauma, Peripheral vasodilation, Anti-hypertensive drugs, Sepsis, Renovascular obstruction, Tumor

PATHO: Diminished perfusion to the kidneys without renal tubular damage
Effect of decreased pressure to kidney perfusion is:Decreased pressure to renal artery, Decreased afferent arterial pressure which diminishes forces favoring filtration, Drop or cessation of GFR -oliguria
Intra Renal Failure***Causes
Causes: True problems of the kidney itself
Polycystic kidney disease (kidney accumulates cysts ), #1 cause of kidney transplant, Diabetes(high blood sugar damages glomerular bed)
Transfusion( accumulate antigen antibody reactions), Severe crush injury (large muscle cells released into circulation leads to clot up glomerular bed), ***Acute tubular necrosis (ATN)( subset of intra-renal failure, look at tubules that are damaged, caused by prolonged ischemia (lack of flow) pre-renal gone bad, Another cause of ATN are nephrotoxic drugs: aminoglycosides (gentamycin, vancomycin), Prolonged sepsis
PATHO: true damage to tissue(infectious process causing decr GFR), Cortical involvement of vascular, infectious or immunologic processes, Causes renal capillary swelling and cellular proliferation
Decrease GFR occurs secondary to obstruction of glomeruli by edema and cellular debris--oliguria
Post Renal Failure
Due to mechanical Obstruction, Bladder obstruction, Anti-cholinergic drugs, Autonomic nerve dysfunction, Infection, Tumor, Uretheral obstruction, Prostatic hyperplasia or tumor
Ureteral obstruction: Blood clots
Calculi, Edema or inflammation, hemorrhage, Surgery (accidental ligation), Tumor, Uric acid crystals
PATHO: complete obstruction: Impediment of urine flow accompanies bilateral kidney involvement, The backup of pressure will compress the kidneys, may lead to intrarenal failure
Acute Renal Failure Clinical Findings
Subjective:
-Irritability; headache; anorexia; tingling of extremities; lethargy and drowsiness that can progress from stupor to coma
Objective:
-Sudden dramatic drop in urinary output appearing a few hours after the causative event
-Restlessness, twitching, convulsions
-Nausea and vomiting
MANIFESTATIONS: Azotemia(Elevated blood urea nitrogen, Elevated serum) creatinine, Metabolic Acidosis(Unable to excrete H+, Unable to conserve bicarbonate, Decrease urine output/
Dilute urine), Electrolyte imbalance, excessive salt/water retention, hyperkalemia, low serum calcium, anemia, low RBC production and lifespan, HTN
TX:Correct the underlying cause of renal failure, Altering medication dosages
Dialysis, Diet therapy-Calories adequated to prevent tissue breakdown: 2000 to 2500 (protein low, high carb for energy, moderate fat), Sodium controlled/Low potassium, Calcium supplements, poss low protein diet-->PREVENT EDEMA SYMPTOMS
DX: ***BLOOD WORK(hyperkalemia, hyponatremia, hyperphosphate, hyopcalcemia, increased BUN, Cr Metabolic acidosis, anemia, fluid overload
Others: Urine (spec gravity/protein), renal ultrasound, CT, IVP, renal biopsy
Chronic Renal Failure
-The progressive inability, over months to years, of the kidneys to respond to changes in body fluids and electrolyte composition with an inability to produce sufficient urine
-Results in gradual tissue destruction and loss of kidney function
-Occassionally results from rapidly progressing disease of sudden onset

Want baseline BUN and Creatinine to see if they came in with it or developed
Can be acute and transform to chronic

PATHO: Gradual loss of entire nephron units, Functional capacity of entire nephron is lost and renal mass is reduced → progressive deterioration of glomerular filtration, tubular secretion and reabsorption, Eventually the kidneys are unable to excrete metabolic waste and regulate fluid and electrolyte balance
Development of CRF
Chronic Renal Failure
1. Diminished renal reserve
-->Nephrons are working as hard as they can
2. Renal insufficiency
-->Nephrons can no longer regulate urine density
3. Renal failure
-->Nephrons can no longer keep blood composition normal
4. End-stage renal disease
*End stage: patient needs dialysis (3 times a week with 5 to 6hr sessions)
MANIFESTATIONS: Hypervolemia
Labs same as ARF, Azotemia, Metabolic acidosis, Anemia, Peripheral neuropathy, Uremic frost
TX: Dialysis, low protein diet, high cal diet, Na/K restriction, fluid restrictions, drugs (loop diuretics, ant htn, sodium bicard, phosph binding agents, ca supp, vit D, Iron, Folic acid, Transplant(last resort)
***Patient who is anemic : definitely needs Fe and folic acid supplements, epogen (stimulate bone marrow and RBC synthesis)
***End stage dialysis and hemodialysis indication for dialysis is potassium
Uremia***
1. Renal filtering function decreases
-->Altered fluid and electrolyte balance
--->Acidosis, hyperkalemia, salt wasting, hypertension
2. Wastes build up in blood
--->Increased creatinine and BUN
--->Toxic to CNS, RBCs, platelets

Increased toxins are causing systemic effects

Mental status changes are signs of uremia Creatinine irritates CNS
Bleed easier because platelets don't work as better
Also, hyponatremia fluid overload

Uremia and hyperkalemia go together
Sets found in the same folder