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Constituents of urinary system
- 2 kidneys
- 2 ureters
Calculus formation at any level of the collecting urinary system. Non-inflammatory. Unknown etiology. Pathogenesis associated with an increased concentration of stone constituents in the urine so that it exceeds their solubility in the fluid (hyper/supersaturated). 10% of Americans. Male predominance.
Chemical content of stones
- 75% calcium oxalate or combo calcium oxalate with calcium phosphate
- 10-15% magnesium ammonium phosphate - triple stones
- 6-23% uric acid salts
- 0.5-4% cystine
Magnesium ammonium phosphate stones
- aka Triple Stones
- formed in alkaline urine (normally it's slightly acidic)
- Alkaline urine more susceptible to bacteria such as proteus vulgaris & other gram negative rods which are part of the normal gut flora & may cause UTI & can convert urea into substances that create an alkaline environment.
- Vegetarians usually have alkaline urine
Uric acid salt stones
- Radiolucent. Sometimes have inclusions of calcium within the stones and will have a patchy appearance on x-ray
- Stones with calcium will always be white on x-ray
Predisposing factors to developing urolithasis
- Urinary obstruction (enlarged prostate, pregnancy, diverticuli)
- Epithelial injury
- Changes in urine
- Quick weight loss
Urinary obstruction leading to urolithasis
slow/no flowing tubes leads to higher chance of precipitation
Enlarged prostate leading to urolithasis
There are 2 lobes in the prostate. The central lobe includes the male urethra. Tumors, etc here can compress the urethra and cause obstruction. The peripheral lobe has low access to the urethra. Tumors here must grow large to be symptomatic.
Benign Prostatic Hypertrophy/Hyperplasia
- located in the central lobes. A smaller amount of fluid causes urination, so there is frequent urination. Because the urethra is narrowed, there may be dribbling, increased abdominal pressure, and inguinal hernias. There is also hesitancy- difficulty initiating urination.
- 70-80% of prostatic carcinoma begins in the peripheral lobes, and is usually caught late.
Pregnancy that causes urolithasis
The fetus can be in a position that compresses the ureter. This increases hydrostatic pressure as the fluid builds up in the kidney (hydronephrosis) and may lead to atrophy of the parenchyma. The capsule around the kidney is very sensitive to pain from distention of the kidneys. Webster's technique can be used to move the fetus as well as having the mom lay on her opposite side. The fetus may also compress veins causing varicose veins, and compress the bile duct causing gall stones
Epithelial injury leading to urolithasis
Epithelial cells slough off & can form a nidus- the organic core of stones. Vitamin A & B6 deficiency causes a reduction in the life span of epithelial cells, so they slough off more often providing more material to form a nidus.
Changes in urine resulting in urolithasis
Dehydration, hypercalcuria, hyperphosphoturia, and oxaluria
Quick weight loss resulting in urolithasis
fat usually surrounds and cushions the kidney. The kidneys distend, which can cause compression of the ureters. Infection may develop- pyelonephritis
Complications of Kidney stones
- Staghorn calculus
- Ureteral Colic
99% are made of magnesium ammonium phosphate (triple stones), & 1% made of cystine. These are large stones formed in alkaline environment. They lead to a dramatic loss of kidney functions and urine flow. Urine will accumulate in the kidney causing distention, hydronephrosis, & atrophy. The parenchyma becomes thin due to increased hydrostatic pressure.
distention of the kidney pelvis with accompanying atrophy of the kidney parenchyma due to obstruction of urine outflow (pressure atrophy). Once complete obstruction occurs, complete atrophy of the kidney will occur & death occurs within 3 weeks. The most common cause of hydronephrosis is kidney stones.
- aka renal colic.
- Full obstruction of the ureter by a stone. Spasm of the smooth muscle walls of the ureter lodge the stone within the ureter. This is very painful, more than child birth. Pain will be in the kidney area & spreads down the flank to the groin, ending in the ipsilateral genitalia. The stone injures the wall of the ureter causing hematuria. There would be a very positive Murphy's punch. Treatment includes pain relievers & muscle relaxers to allow the stone to move. If the stone is too large, they can surgically remove it.
More common in males over 60 years old. They are oval shaped & a different size than kidney stones. An instrument is inserted into the urethra to remove the stones. No anesthesia is used because the Dr could tear the male urethra near the prostate. It is less painful for women because they have a shorter, wider ureter.
inflammation of the urinary bladder. Usually occurs in females. Usually caused by an infection from the normal gut flora.
Causes of acute cystitis
- E. Coli- #1 cause
- Other gram negative bacteria
- STD's like gonorrhea & chlamydia
- Yeast infection- Candida albicans aka monila. Sometimes called candidosis or moniliasis. The normal flora suppresses candidosis. Common in the US b/c of antibiotic use in cattle & over prescribed antibiotics. Antibiotics suppress the normal flora. There will be a curd like vaginal discharge. Buttermilk stimulates the gut flora
Predisposing Factors of Acute Cystitis
- Exposure of the female pelvis to cold. Ovaries are anatomically hidden to keep them at the proper temp. They are very sensitive to cold. Vasoconstriction decreases blood flow, temp goes down, there is decrease in function of enzymes & increase in infection. The healing process forms connective tissue that will shorten & narrow the lumen of the fallopian tubes leading to tubal pregnancy or infertility.
- Pouches in bladder (especially if urine is sweet)
- Foreign bodies within the bladder
Major symptoms of acute cystitis
- Dysuria-painful urination
- Increased frequency of urination
- Lower abdominal or suprapubic pain (lower than umbilicus)
- The above symptoms must ALL be present to indicate cystitis. If one is missing it is NOT cystitis & could be pelvic subluxation
- Hematuria may or may not be present
Treatment for acute cystitis
Involves antibiotics. Improvement should occur within a day. If there is no improvement within 3 days, it is not cystitis. Antibiotics should be taken for at least 7 days. If not, it may lead to chronic cystitis which reduces the bladder capacity & is incurable.
Retroperitoneal organ that encircles the neck of the male bladder & urethra. 20 grams. Devoid of distinct capsule. Divided into 4 zones. Peripheral (where most carcinoma arises), central, transitional (where most hyperplasia occurs), & the periurethral zones. Has 2 cell layers, the basal layer made of cuboidal epithelial cells, & the covering layer made of columnar secretory cells.
3 major pathological problems that involve the prostate
- benign nodular enlargement (most common in aging)
inflammation of the prostate
Acute Bacterial Prostatitis
caused by UTI, usually E coli, enterococcus, staphylococcus, or other gram negative rod bacteria. Due to intraprostatic reflux of urine & may follow surgical manipulation of the urethra or prostate, like catheterization, cytoscopy, urethral dilation, & prostate resection. Symptoms include chills, fever, & dysuria. Rectal exam will show an extremely tender boggy prostate
Chronic Bacterial Prostatitis
difficult to diagnose. Diagnosis is dependant upon positive cultures, & history of recurrent infections (cystitis, urethritis). Symptoms include insidious onset of low back pain, dysuria, & perineal/suprapubic discomfort. Antibiotics will not be effective.
Chronic Abacterial Prostatitis
MC form of prostatitis. No history of recurrent infection. Leukocytes will be present in the urine, but bacteria will not.
common procedure in US, instill bacillus for superficial bladder cancer. There is also a fungal type which occurs only in immunocompromised patients. The relatively common nonspecific type is a reaction to secretions from a ruptured prostatic duct
Nodular Hyperplasia aka Benign Nodular Hyperplasia
- Extremely common disorder for men over 50. 20% of men by the age of 40, 70% of men by 60, 90% of men by the age of 70. 50% of men have symptoms. Involves hyperplasia of the stroma & epithelial cells forming a large discrete nodule that compresses the periurethral zone which narrows or obstructs the urethral canal.
- Etiology- the prostate synthesizes dihydrotestosterone from circulating testosterone which controls the prostates growth
Symptoms of Nodular Hyperplasia
- Difficulty urinating due to compression of the urethra
- Retention of urine which causes bladder distension, hypertrophy, urinary infection, cystitis, & renal infection (hydronephrosis, azotemia, uremia)
- Difficulty starting & stopping urination
Treatment of Nodular Hyperplasia
Surgically by transurethral resection, alpha blockers, reduced fluid intake at bedtime, decreased intake of alcohol & caffeine, & phytochemicals.
Adenocarcinoma of the Prostate
MC form of cancer in men & the 2nd leading cause of cancer deaths. Typically affects men over 50, uncommon in Asians & MC in US black males. Unknown etiology, but may be associated with diet & genetics. A common genetic alteration is hypermyelination of glutathione S-transferase gene promoter (GSTP-1). It will be palpable during a rectal exam due to the typical posterior location on peripheral zone. It will feel gritty and firm. Spreads locally or through the bloodstream or lymph. May involve the seminal vesicles & the base of the urinary bladder. The blood will spread to the axial skeleton.
Gleason Grading System
- 5 grades based on glandular pattern & differentiation
- Grade 1- well defined tumor
- Grade 5- no glandular differentiation
- Primary & secondary dominant patterns are graded then added together. 5-7 is treatable, 8-10 is untreatable.
Prostatic Specimen Antigen
- used in diagnosis. It is a product of the epithelium & is organ specific, not cancer specific. Useful for treatment response
Treatment of Adenocarcinoma of the Prostate
Stomach digests proteins (carbs begin to digest in the mouth & fat in the duodenum), produces some hormones, & stores food. It is located in the upper left abdominal cavity above the ribcage, the epigastric area
Fundus of stomach
small area at the top of the stomach where gas accumulates & is seen as a gastric air bubble- if gas gets in vessels, blood stops flowing
Lesser curvature of stomach
on the medial side & is a common site for peptic ulcers & cancer
Cardia of stomach
Contains the gastroesophageal junction closed up by the cardiac sphincter. The sphincter normally prevents the stomach contents from backing up into the esophagus, b/c the mucosal tissue of the esophagus is very sensitive to stomach acid. If the stomach contents back up into the esophagus due to an improperly working sphincter you get heartburn. Chronically this can lead to esophageal cancer- Barrett's esophagus.
Antrum of stomach
Small triangular area at the bottom of the the stomach that contains the pyloris. The pyloric sphincter regulates how much content can move from the acidic stomach to the alkaline duodenum. The most common site for peptic ulcers is the duodenal bulb
Distension of the stomach
Can lead to abnormal placement of the stomach within the stomach cavity - hypotonic or atonic
Rugae of stomach
Folds in the stomach wall. It is folded to increase surface area. The stomach wall is very thick with deep pits covered with columnar epithelial cells without goblet mucus producing cells. If goblet cells are found in the stomach, it is usually a sign of stomach cancer. The stomach has mucosal glands deep within the pits that produce mucus that acts as a protective barrier against acid.
1 billion in the stomach that produce HCl & intrinsic factor. The HCl breaks peptide bonds, prevents intestinal infections, & activates pepsinogen to pepsin
3 stimulators of HCl
- Neural by vagus nerve (parasympathetic)
- Endocrine by gastrin
- Histamine is a local stimulator. It is found in mast cells. Eating spicy foods will cause degranulation of mast cells.
for absorption of vitamin B12 in the ileum. Deficiency in B12 is called pernicious anemia. Pernicious means malignant. Pernicious anemia is a megaloblastic anemia (immature RBC's) meaning the blood cells are large (macrocytes), & have a rigid membrane that prevents them from bending to get out at the capillaries. Neutrophils & other WBC's are hypersegmented with more than 5 nuclei. There is CNS damage of the posterior columns of the spinal cord. With the folic acid deficient anemia, the CNS is spared (except in fetus)
- aka Chief cells
- Produce pepsinogen which is inactive. Pepsinogen is activated by HCl to pepsin(& keeps it in this form - major physiological function).
- The zymogen cells would be damaged if the produced activated pepsin
located in the antipyloric area & produce gastrin, the endocrine stimulator
chronic mucosal inflammatory changes of the stomach wall that eventually result in mucosal atrophy & metaplasia
Cause of chronic gastritis
H Pylori, a gram negative rod. 50% of Americans have H pylori in their stomach & 80% of Russians & Puerto Ricans do. H pylori produces metabolites that are toxins or enzymes that are harmful, causing atrophy of the mucosa. The stomach epithelial cell may transform into intestinal epithelial cell- metaplasia predisposes you to cancer, intestinal type adenocarcinoma.
Why should predisposition to cancer be checked yearly?
- To be caught early of cancer develops
- The stomach walls become thinned, & sometimes the blood vessels are damaged. Hemorrhaging in the stomach will produce black stool, melena. Iron reacts with the HCl & forms iron chloride, which has a black color. There may be stomach pain, belching, poor appetite, anemia, bad mood, heaviness of the left side, & signs of malnutrition.
More typical in Scandinavian countries. The parietal cells are selectively damaged. Leads to vit B12 deficiency b/c less intrinsic factor is produced. They will have hypo acidity & megaloblastic anemia
lymphadenopathy of the supraclavicular lymph nodes called virchow's nodes, due to either stomach or lung cancer
There are 2 major types that make up 95% of all stomach tumors. Intestinal type adenocarcinoma & diffuse stomach carcinoma. Stomach cancer is more common in the lesser curvature.
Diffuse stomach carcinoma
More common than intestinal type carcinoma. Involves entire stomach wall. Short latent period before it metastasizes & often comes to clinical attention late. Risk factors are unidentified & H Pylori & chronic gastritis is usually absent. Schirrous cancer (i.e. Breast adenocarcinoma-invagination of nipple), made mostly of stroma (CT-up to 90%). The stomach shrinks b/c of the connective tissue. Sometimes called leather bottle stomach or linitus plastica b/c the stomach is rigid & can't distend.
Intestinal type adenocarcinoma
Less malignant than diffuse stomach carcinoma. Has a long latent period. Has many predisposing factors. Tumor projects into lumen of stomach
Predisposing factors of intestinal type carcinoma
Infection with H. pylori, diet (nitrites, smoked food, salty food, pickled food, lack of fruit & vegetables), smoking, chronic gastritis, partial gastrectomy, gastric adenomas (40% cancerous at time of diagnosis, 30% have adjacent cancer at time of diagnosis), Barrett esophagus, family history
chance of benign stomach polyps becoming mailgnant
become malignant 4% of time
chance of colonic polyps becoming malignant
become malignant 40% of time
stomach cancer that spreads through the abdominal wall cavity to the ovaries--> secondary ovarian cancer
benign tumor from smooth muscle
How stomach cancer or cancer of the GI tract metastasize to liver
- Via portal system. Carries cancer cells in blood from stomach to liver
- (usually cancer metastasizes thru lymph vessels)
Diagnosis of stomach problems
- Epigastric pain less than 30 minutes after a meal indicates stomach cancer
- Epigastric pain 30 minutes -1 hour after a meal indicates stomach peptic ulcer
- Epigastric pain 1 to 3 hours after a meal indicates duodenal peptic ulcer
heart attack - indicates the development of an area of myocardial necrosis caused by local ischemia
Transmural Myocardial infarct
Involves the entire thickness of the heart wall
Intramural myocardial infarct
- Only affects a portion of the thickness of heart wall
- (subendocardial more vulnerable than subpericardial)
Good. Preserves shape, size, & strength for several days to allow healing
reduction in speed of blood flow leads to:
thrombosis- forms in connective tissue of heart because it doesn't contract
2 causes of myocardial infarcts
- Coronary artery spasms
- acute thrombosis
Single blood supply
more than 1 blood supply (lung- pulmonary & bronchiole)
Exudate accumulation due to inflammation
Why are younger myocardial infarct patients at a higher risk of death than older victims
No atherosclerosis. No anastomoses to keep feeding heart
accumulation of fluid in pericardial space. Heart can contract, but can't relax. Fatal- postnephrotic syndrome
Rupture of interventricular system
blood mixes in right ventricle (lower pressure)
pouching of wall of heart (transmural infarct)
Due to renal, endocrine, vascular, neurogenic
Benign tumor of adrenal medulla - epinephrine & norepinephrine - vasoconstriction - increased BP
Adrenal cortex- tumor of cells that produce aldosterone- primary hyperaldosteronism - Na reabsorption - water reabsorption - increased BP
- Development of diagnosis in proper time (> 45 yoa)
- Slow increase of BP during years
- BP can be controlled by healthcare provider
- Any age vulnerable
- Very high numbers.
- Rapid progression (death within a year or two)
- Cannot be controlled by healthcare provider
The patholomorphological foundation of malignant hypertension is
Idiopathic Inflammatory Bowel Disease
Chronic inflammatory conditions w/ inappropriate & persistent activation of the mucosal immune system. There is chronic relapsing of these inflammatory disorders that have an obscure origin. There will also be extraintestinal inflammatory manifestations. The homeostasis of the normal intestinal flora is disrupted by a strong immune response against the normal flora. There is too much T-cell activation (CD4+). There are defects in the epithelial barrier function. Usually involved a genetically susceptible individual & is associated with NOD2 protein mutation. Diagnosis cannot be determined by a single test, it's dependent on the history, x-rays. labs, & tissue pathology exams. 2 types: Crohn's & ulcerative colitis.
autoimmune disease affecting any portion of the GI tract w/ a chronic delayed-type hypersensitivity reaction. Often involves the distal small intestine & colon (small intestine 40%, colon 30%, small intestine & colon 30%). Affects females slightly more than males. Whites 2-5x's more & Jews 3-5x's mores. Smoking is exogenous factor. Symptoms are aggravated by physical & emotional stress. Increased incidence of GI tract cancer
Morphology of Crohn Disease
Intestinal walls become rubbery and thick with edema, there are skip lesions where there is a gap between affected segments and unaffected segments, there are narrow fissures between mucosal folds, fistula formations, presence of noncaseating granulomas, mucosal inflammation, chronic mucosal damage leading to metaplasia, ulcerations, & fibrosis & hypertrophy of the mucosa.
Symptoms of Chron's disease
Mild diarrhea, fever, abdominal pain acutely in the lower right quadrant, fecal blood loss results in anemia, & there may be malabsorption of bile salt and loss of albumin. There are asymptomatic periods.
Extraintestinal Manifestations of Chron's disease
clubbed fingernails, ankylosing spondylitis, migratory polyarthritis, sacroilitis, uveitis, hepatic involvement, & skin lesions.
Chronic inflammatory disease limited to the colon and rectum. Affects white females more peaking b/w 20-25 years old. Affects nonsmokers and ex-smokers more than smokers. It is aggravated by physical or emotional stress.
Morphology of Ulcerative Colitis
Affects the mucosa and submucosa in a continuous fashion, granulomas and fistulas are absent, ulceration of the mucosa throughout, & pseudopolyps- regenerating mucosa
Symptoms of Ulcerative Colitis
Persistent bloody diarrhea, fever, lower abdominal pain, cramps relieved by defecation. There are asymptomatic periods.
Outlook of Ulcerative Colitis
Depends on severity and duration. 97% have a relapse in 10 years, 30% require a colectomy in 3 years of onset. The major complication is cancer, so screening is essential