M10: Renal/GI Flashcards

1
Q

Pyelonephritis

A

A type of UTI that has reached the pyelum (pelvis) of kidney.
ascending infection: some type of vesicoreflux dysfxn. or instrumentation
MC female
CM: fever, sudden onset, flank Pain, uti s/s (dysuria, freq, urgency)
DX: cbc (leukocytosis), BUN/CR, **UA w/ micro and C&S; white cell casts (renal cause for pyuria & has reached renal tubules)
imaging: CT ABD w/ or w/o
TX: abt-adjusted for bacteria, most will improve on their own

renal fxn not @risk d/t only 1 kidney affected.

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2
Q

Obstructive renal disease- what does it cause?

A

Obstructive renal disease causes a blockage in the urinary tract that impedes the flow of urine, leading to urine accumulation and kidney damage.
anatomic or functional
severity based on:
Location, completeness, involvement of one or both upper urinary tracts, duration, and nature/cause

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3
Q

Upper Urinary obstruction complications

A

Hydroureter: dilation of ureter
Hydronephrosis: dilation of renal pelvis & Calyces (swelling of kid.
Ureterohydroneph: dilation of both ureters, renal pelvis and calyces
Tubulointerstitial fibrosis: depsoition of excessive amoutns of extracelluar matrix

Leads to excess cellular destructions and death of nephrons

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4
Q

Renal calculi (AKA nephrolithiasis) causes

A

crystals, protein and mineral salts from uro tract form masses/stones
calcium oxilate and ca phosp=70-80%
Struvite (infectious) from UTI-stone from MG, Ammonium, and PHos
Uric acid/cystine 5-10% (pink stone)
Staghorn calculi: large and fill the minor and maj calyx’s
RF: male (doubled), most before age 50, inadeq po fluid intake, geo location, familial hx
diet heavy in: rhubarb, spinach, chocolate, nuts and beer.
<5mm will resolve on own
DX: U/S, CT, UA w/ micro
s/s: renal colic (d/t dilation), dull/local flank pain; n/v/d, pale, cold sweats
*huge sympathetic response
Tx: hydration to reverse precipitation, potass. citrate, ca channel blockers, and alpha adrenergic blockers, lithotripsy, surg w/ stents

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5
Q

Urinary Tract Obstruction - most common cause

A

MC cause of a urinary tract obstruction is renal calculi.

tumors
enlarged prostate
neurogenic bladder
urethral stricture
pelvic organ prolapse

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6
Q

UTI:
**Bacturia
Pyuria (WBC in UO)

A

can be complicated vs non-comp.
comp: asso w/ structural d/o

MC Pathogen: E coli and staph saprophyticus (found in fecal flora)

Virulence: evade host defense, adherence to uroepithlium (have pili or fimbraie or both), biofilms to resist host mechanisms.
DX: midstream UA w/ micro

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7
Q

Urinalysis: application scenario

A

Urinalysis is crucial in diagnosing UTIs, including pyelonephritis, by detecting the presence of bacteria, white blood cells, or pus in the urine.
UTI-UA micro
10 leukocytes/microliter
>5 RBC’s
gram stain
>1, 000 colony forming unit (CFU) if <1K=contamination

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8
Q

Mechanisms that protect the
urinary tract from infection
include
1. monocytes in the urine.
2. acidic urine.
3. decreased urine osmolarity.
4. type-I pili.

A
  1. acidic urine pH=1.0

low pH reduces likelihood of infection

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9
Q

Innate defenses against UTI (think urine composition)

A

Urine composition plays a vital role in preventing UTIs.
urine’s acidity,
the presence of urea,
various immune proteins help deter bacterial growth.

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10
Q

NephrOtic

A

proteinuria >3.5gm (from glom injury)
decr albumin= decr plasma oncotic pressure=severe edema
causes: damage to basement membrane and podocytes of glom.
C/B: systemic ds (lupus, dm, amyloidosis)

Tx: low protein diet (incr will do more harm), low fat diet, NA restrict , diurectics, glucocorticoids, ARBS

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11
Q

Nephrotic syndrome produces
1. sodium loss.
2. protein retention.
3. susceptibility to infection.
4. IgA nephropathy

A
  1. susceptibility to infection:
    loss of proteins via the basement membrane, includes loss of immunoglobins
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12
Q

Nephritic

A

Gross hematuria w/ sudden onset
RBC casts in urine
s/s: small azotemia, edema, htn, oliguria
C/B: incr permeability of Glom filtration membrane
50% of adults will progress to ESRD in 10-20 years after onset

linked to strep infections

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13
Q

Causes of acute renal injury and nephritis

A

Acute renal injury can be caused by severe or sudden kidney damage. w/ decr in GFR & accum of nitrogenous waste.
incr CR/BUN

Pre-renal: hypoperfusion MC
Intrarenal: d/o involving parenchymal or interstitial tissue OR actue tubular necrosis (ischemia) (ATN)
Postrenal: rare; d/o asso w/ acute obstruction.

Nephritis is often caused by infections, toxins, or autoimmune diseases affecting the kidneys.

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14
Q

Individuals with chronic renal failure often develop
1. hypocalcemia.
2. macrocytic anemia.
3. increased
erythropoietin
secretion.
4. metabolic alkalosis.

A
  1. hypocalcemia
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15
Q

Stomach anatomy and production of what substances
4 areas of stomach

A
  1. Cardia: lined by mucin secreting Foveolar cells
  2. Fundus: houses glands that contain chief cells which use & produce digestive enzyme: Pepcin
  3. Body: has similar glands, also produce pepcin
  4. Antrum: similar to foveolar cells, but contain endocrine cells (G cells) that secrete Gastrin which stims gastric secretion.
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16
Q

Gastric secretions-Hydrochloric Acid

A

Converts pepsinogen to pepcin

Stims: acetylcholine, caffeine, CA, Gherlin, Gastrin, and Histamine

Inhibits: Atrial naturetic peptide (ANP), cholecystokinin, GLP-1, somatostatin, Secretin, Prostaglandins.

17
Q

Intestinal digestion/absorpt.

A

Carb–mono/disaccharides
Proteins degraded to aminoacids & peptides
Fats emulsified- fatty acids, monoglycerides

18
Q

Non alcoholic fatty liver disease (NAFLD)- associated with?

A

NAFLD is associated with obesity, type 2 diabetes, hyperlipidemia, and metabolic syndrome.
**

19
Q

A person has alcoholic liver
disease. What is the sequence for
the development of this disease?
1. Incubation, prodromal, icteric,
and recovery
2. Prehepatic, intrahepatic, and
extrahepatic
3. Steatosis, steatohepatitis, and
fibrosis
4. Overflow, underfill, and
peripheral artery vasodilation

A
  1. Steatosis, steatohepatitis, and
    fibrosis
20
Q

Hepatic encephalopathy physiological marker/lab analysis

A

Acute: incr ammonia levels

Chronic: change in neurotransmitters over time
impaired cog, behavior, and motor fxn
CM: personality changes, confusion, irritablitity, lethargy, flapping tremor (asterixis), rigidity, EEG changes.

Tx: correct elyte imbalances,
w/d depressant drugs metabolized in liver, restrict dietary protein intake, hypertonic/manitol, hypothermia.
elliminate GI bacteria: neomycin, lactulose, glutamase inhibitors, rifaximin.

21
Q

Intestinal surgery emergencies - highest occurrence

A

Intestinal obstruction is one of the highest occurrences leading to emergency intestinal surgeries. Causes include adhesions, hernias, and tumors.

22
Q

Causes of GI ulcers & Chronic NSAID sequela 

A

break/ulceration in protective mucosal lining of lower eso, stom, duoden. d/t ischemia
Chronic NSAIDS inhibit prostaglandin production which damages mucosa.
RF: genetics, H. pylori, etoh/smoking, copd, obesity
H pylori in 70% of cases, but only 5-10% will dev. ulcers
3 mil. are tx’d each year, 5,000 deaths/yr
MC w/ hx of gastritis and chr inflam.

80% will occur in dudenum-mc w/ smokers; s/s: epigastric pain postprandial, tx: PPI, H-2 blockers, anticholenergics

23
Q

Gastric secretion phases and digestion process begins where?, procedure of swallowing is controlled where?

**

A

Digestion begins in the mouth with salivary amylase breaking down carbohydrates.
**
The process of swallowing is controlled in the brain, specifically the medulla oblongata.

24
Q

Dysphagia:

A

mechanical vs obst
Achalasia: denervation of sm m in eso, leading to lack of lower eso sphincter (LES) relaxation

*predisposition to eso ca

*increase risk for ASPiration PNA

25
Q

Projectile vomiting

A

Projectile vomiting can be a sign of increased intracranial pressure, gastrointestinal obstruction, or a severe form of pyloric stenosis.

Spontaneous, does NOT follow N/retching

26
Q

GI Bleed terms

A

Upper: coffee ground emesis/stool
Lower: from jejun, ilieum, colon or rectum

Hematemesis: bloody vomit
Hematochezia: bloody stools
Melana: black, tarry stools
occult bleeding: not visible.

27
Q

Esophageal Varices

A

Asso w/ liver ds, esp pHTN
esophageal BV dilation
Tend to rupture, if they do 50/50 chance of death, w/ 1/2 of these are w/ advanced cirrhosis

28
Q

Lab tests for monitoring progressive renal function

A

Key laboratory tests include serum creatinine, blood urea nitrogen (BUN), and estimated glomerular filtration rate (eGFR) to monitor renal function.

29
Q

Colon cancer lab abnormalities for new diagnosis

A

Lab abnormalities that may indicate colon cancer include elevated carcinoembryonic antigen (CEA) levels, anemia (low hemoglobin), and potentially altered liver enzymes if metastasis has occurred.

30
Q

renal tumors
benign 40%
RCC=renal cell carcinoma MC

A

RCC-“silent Ca” as symptoms go unrecognized until tumor is large.
from epithelial cells in proximal convulted tube, MC: polyglonal epith. cells
mutation of the von Hippel-Lindau (VHL) on Chromo 3p25
CM: heaturia, dull/ache flank pain, palpable flank mass in thin individuals
EPI: older men

Bladder: Urothelial ca MC (TP53 mutation)
RF: smoking, aromatic amines, arsenic in water, cyclophosphamide, pioglitzone
TX: TURBP, radical cysto w/ diversion, chemo/rad: cisplatin-based

31
Q

Zollinger-Ellison Syndrome (GI)

A

tumor of gastrin cells=uncontrolled gastrin content