NRSG 326

cholelithiasis

-stones in the gallbladder

-devels when bile salts, cholesterol & calcium system is out of balance

-most common biliary system disorder

-genetics, diet, medications (OCPs)

-incidence: 10 000/100 000 (not accurate bc can have asymptomatic)

choledocholithiasis

-stones in the common bile duct

-if obstructed, no bilirubin reaches sml intestine --> no urobilinogen in urine

cholecystitis

-inflammation of the gallbladder

-commonly associated with gallstones

-bile/pus distension, duct occlusion

-acute: gb is edematous & hyperemic, scarring

-chronic: tissue fibrosis --> decr'd gb fnctn

pancreatitis

-acute inflammation of pancreas

-pancreatic enzymes spill into self "auto-digestion"

-very painful!

-most common cause: ETOH misuse, cholelithiasis

-incidence: 5-35/100 000

gallbladder disease risk factors

cholelithiasis, cholecystitis

-XX, multiparous, >40yrs, estrogen Tx, sedentary, genetics, obesity, Indigenous ppl

oral contraceptives & gallbladder

-OCPs alter bile --> incr'd cholesterol saturation --> potential incr'd risk for gall stones

symptoms of gb disease

-fever, tachyc, hypoT

-indigestion, N/V

-mod-severe pain, RUQ

-jaundice

pancreatitis diagnostics

-gold standard: elevated serum amylase level (3x normal)

-elevation of serum lipase

-high glucose

-low calcium (goes intracellular --> tetany)

-WBC, lytes

cholecystitis/cholelithiasis diagnostics

-LFT (AST, ALT, ALP, GGT)

-bilirubin

-WBC

-lytes

-abdo XR/US, CT scan

-U/S: esp helpful for jaundice pts & ppl allergic to contrast

urobilinogen

-bilirubin broken down in intestine & becomes this colourless compound

-excreted mostly in feces, some reabs'd that kidneys excrete

-higher/lower urobilinogen in urine --> liver disease, hemolytic anemia, biliary obstruction

complications of gb disease

-gangrenous cholecystitis

-subprhenic abscess

-acute pancreatitis

-cholangitis (bile duct inflam)

-choledocholithiasis (bile duct stone)

-biliary cirrhosis

-hypoglycemia

-ileus

-sepsis (from necrosis)

-fistulas

abdominal compartment syndrome

-gb rupture (bile peritonitis)

-cancer

abdominal compartment syndrome

-increase in abdominal pressure to point where arterial b flow is blocked --> tissue ischemia --> organ dysfunction

total obstruction symptoms (gb)

-obstructive jaudice

-dark amber urine

-clay-coloured stools

-pruritis

-bleeding tendencies

cholecystitis Tx

-analgesics - ketorolac (visceral pain)

-abx - levofloxacin

-fluid & lyte balance

-gastric decomp. (severe N/V)

-anticholinergics (atropine- decr secretions, reduce sm musc spasms) NOTE if ileus present, will worsen!

-*lap chole (Tx of choice)

cholelithiasis Tx

-analgesics - opioid, NSAIDs (if kidneys ok)

-fat-sol vits ADEK

-bile salts

-cholestyramine (bile binder for pruritis) (mix w/ milk/juice)

-extracorporeal shockwave lithotripsy, ERCP stone removal

-*lap chole (Tx of choice)

pancreatitis Tx

-analgesics

-BG monitoring

-*chronic pancreatitis: need to replace enzymes i.e. pancrelipase, insulin

-ERCP

-lap chole

-percutaneous drain

contraindications of lap chole

-peritonitis

-cholangitis (bile duct infxn)

-gangrene or perforation of gb

-*portal HTN

-serious bleeding disorders/coagulopathy

pt education for gb disease/pancreatitis

-avoid/decr ETOH

-diet mods: high fibre, low sat-fat diet (d/t cholest. stones), low-cal if obese; small freq meals

hepatitis

-inflammation of the liver

-viral is most common

other types: ETOH, autoimmune, other viruses (rubella, EBV, cytomegalo, coxsackie, herpes)

Hep A + high risk popus

-fecal-oral route; poor hygiene, improper food handling, crowding, institutionalized ppl

-drug users

-MSM

-ppl in close contact, poor sanitation

-travellers to endemic areas

Hep B + high risk popus

-blood, bodily fluids

-baby born to HBV mother

-ppl in high prevalence areas

-injection drug users

-ppl w/ mult. sexual partners

-inmates

-HCWs & 1st resonders

Hep C

-bloodborne, "risky" behaviours, needle-sharing

-injection drug users

-ppl w/ tattoos from unreg. settings

-recipietns of b transfusions pre 1992

-incarcerated/long Hx

-ppl of Indigenous descent

Hep D

-blood, body fluids

-req's HBV's presence to replicate

Hep E

-fecal-oral

hepatitis: stages of progression

-healthy liver -> acute inflam -> chronic inflam (all reversible) -> cirrhosis (permanent damage- life expectancy shortens) -> end stage (terminal)

-*Hep A is only viral one to allow for full recovery - others do not bc of damage to hepatocytes; 80% HBV and HCV lead to chronic infxn

Hepatitis nrsg assessment

-IV drug use, ETOH misuse

-wt loss/gain

-dark urine

-fatigue

-RUQ pain

-pruritis

-low-grade fever

-jaundice

-abnormal labs

what level of serum bilirubin req'd to detect jaundice

-35 mcmol/L

Hep B acute Tx

HBIG hep B immunoglobulins

-used post-exposure

-contains antibodies to help fight virus

-*GIVE w/in 24hrs of exposure*

Hep B chronic Tx

nucleoside analogues:

-entecavir PO for 1yr minimum

-inhibs viral DNA synth ONLY when active

interferon:

-decr viral load, liver enzymes

-decr rate of disease progression

-SC Qweek for 48 wks

-SEVERE rxns possible

Hep C chronic Tx

Maviret (glecaprevir/pibrentasvir):

-decr viral laod, redaicate virus

-decr progression of disease

-3 tabs PO daily for 8-16wks

Hepatitis prevention

HAV:

-pre-exposure vaccine IM

-Ig pre- or post-exposure

-temporary passive immunity

HBV:

-pre-exposure vaccine IM

NO VAX for hep C/D/E

what to manage with decomp'd cirrhosis

-ascites

-varices

-encephalopathy

-infxn prevention

-NO ETOH

-no judgement

liver blood flow

hepatic artery (aorta to liver, O2 rich)

hepatic portal vein (GI to liver- nutrient rich, O2 poor)

hepatic vein (liver - IVC, O2 poor)

inferior vena cava -> R atrium

fnctns of liver

-blood filtration: toxin removal

-RBC breakdown

-bile production

-metabs proteins, CHOs, fats

-makes albumin

-prods clotting factors (vit K etc)

-regs amount of blood circulating

-stores glycogen & vits

-metabs sex, thryoid, adrenal hormones

-metabs mineralocroticoids & glucocorticoids

-produces angiotensinogen (RAAS)

-metabs & activates meds

alcohol-associated liver disease progression

steatosis -> alcoholic hepatitis -> alcoholic cirrhosis

steatosis

-fatty liver

-*reversible: high AST, ALT, lipids, GGT

alcoholic hepatitis

-inflam from ETOH -> hepatocyte injury, fibrosis

-*possibly reversible IF caught early

-*jaundice, high AST, ALT, ALP, bilirubin, INR

alcoholic cirrhosis

-permanent scarring

-compensated vs decompensated

non-alcoholic fatty liver disease progression

steatosis -> non-alcoholic steatohepatitis -> cirrhosis

-*NOTE: non-alc. liver disease MORE common than ALD*

compensated cirrhosis + s/s

-normal liver fnctn & bloodwork despite severe hepatocyte injury

-s/s: fatigue, abdo pain, anorexia, dyspepsia, weakness, musc atrophy

decompensated cirrhosis + s/s

-hypoalbuminemia -> ascites

-prolonged PT/INR

-portal HTN -> bleeding, spider angiomas (estrogen-rel'd), esophageal varices

-elevated bilirubin: jaundice, dark urine

-incr ammonia: encephalopathy, asterixis (flapping tremor)

-gynecomastia (d/t decr/no estrogen clearance)

hepatorenal syndrome

-occurrence where kidney fnctn declines rapidly in advanced cirrhosis

-assoc. w/ SUDDEN oliguria, decline in kidney fnctn, ascites

-only LT cure is liver tsplant 60% survival in 3 yrs

-NO liver tsplant: 50% die in 90days

ESDR (end-stage renal) s/s

-proteinuria, oliguria, anuria

-hyperkalemia

-elevated BUN, Cr

-decr GFR

-metabolic acidosis

-hypocalcemia

-uremic frost (skin)

-pericarditis

-msuc cramping

-HTN

ESDR & liver failure same s/s

-fatigue

-anorexia, N/V

-pruritis

-peripheral edema

-peripheral neuropathy

-high JVP: hepatojugular reflex

decomp'd cirrhosis

-chronic inflam that causes extensive fibrosis nodules after trying to repair itself

-ETOH, non-ETOH, autoimmune, viral

-mgmt: stop ETOH, decr dietary fat, tsplant

acute liver failure: onset, key s/s, causes, Tx

-acute onset: 8 wks

-*rapid encephalopathy, INR >1.5

-no known liver disease

-causes: meds, ETOH, drug rxn, viral hepatitis, HELLP syndrome, fast-growing CA, ischemia, mushroom poison, sepsis, heatstroke, wilson disease, budd chiari (narrowing of hepatic veins)

-Tx: ICU & tsplant

hepatic encephalopathy

-impaired ammonia metab -> neurotoxic fx; inflam cytokines

-s/s: cerebral edema, LOC change, memory loss, asterixis, impaired handwriting, hyperventilation w/ resp alkalosis, pos bobinski (toe flare)

-Tx: lactulose, low protein, safety, rest, rectal tube

ascites paracentesis

-removal of XS abdo fluid

-can remove up to 5L w/out admin of IV albumin

portal HTN

decreased blood flow through the liver -> HTN in portal circulation

-causes ascites, peripheral edema, splenomegaly, varices (esophageal, caput medusae)

if varices rupture

-life threatening emergency d/t hemorrhage, airway risks - call for help

-maintain airway and circulation

-ensure IV access (i.e., for emds, fluid, blood admin)

-Tx: balloon tamponade w/ 3-way cath., scleropathy, banding

CKD

-progressive, irrevesrible loss of kidney fnctn

-stages are delineated by eGFR -<60mL/min/1.73m2 for 3+ mos

-1/10 CADs have kidney disease, 1/3 FNs

stages of CKD

-normal GFR ~125mL/min

-stage 1: GFR >90

-stage 2: GFR 60-89

-stage 3: GFR 30-59

-stage 4: GFR 15-29

-stage 5/ESRD: GFR <15

KDIGO Guidelines

International guidelines for kidney disease management

-compares GFR (in stages G1-G5 & 3a/b) to categories of albuminuria (A1-A3)

CKD causes

1. diabetes d/t high sugars passing thru nephrons

2. HTN/renal-vasc disease d/t high pressure on kidneys

3. glomerulonephritis

4. polycystic kidney disease

5. pyelonephritis

kidney fnctns

-filter waste prods (urea - byprod. of protein metab.)

-maintain fluid, lytes, acid/base balance (K+, H+, ammonia)

-excrete metab. wastes

-reg BP & bone density

-produce EPO (if low O2, low b flow)

-activate vit D

-secretes renin (RAAS)

-secretes aldosterone (regs K+/Na+)

-regs Ca2+/PO4+

aldosterone & kidneys

-incr Na+ and H2O reabs. in DCT; Spironolactone inhibits

PTH & kidneys

-PTH causes tubular Ca2+ reabs. and incr phosphate excretion

diet for someone with CKD

-low Na+ (<2g/day), K+ (beans, nuts, dried fruits), phosphorous (meat, dairy prods), protein

CKD diagnostics

-CBC

-urinalysis

-lytes

-eGFR, Cr

-renal US

meds/supplements for CKD pts*

-phosphate binders (incr Ca2+, decr LDLs; watch C)

-vit D (Ca2+ absorption, decr PTH)

-calcimimetics (cntrl parathyroid)

-EPO (incr Hgb, HCT in 2-3wks; watch HTN*)

-Fe+ (if <100ng/mL

-folic acid/vit B9 (RBC formation) - removed by dialysis

-NOTE: ensure all nephrotoxic drugs switched, D/C i.e. enoxaparin -> heparin

nephrotoxic meds

-NSAIDs

-aminoglycosides

-ACE inhibs

-glycopeptides (i.e. vancomycin)

-lithium

CKD: hyperkalemia Tx

*if >5.5: kayexalate*

-exchanges K+ for Na+

-KEEP commode nearby

*if >6: insulin*

-can lead to tall, tented T-wave

* if >6.5 + ECG changes*

-remove K+ from b stream

-IV insulin & glucose

-B2 agonist (i.e. salbutamol)

lasts 2 hrs so kayexalate can work, ICU transition

kardex of CKD pt

-I/O

-daily wts

-bloodwork daily (CBC, lytes, Cr, eGFR, urea, BUN)

-urinalysis or 24hr urine (albumin)

-renal diet

-nephrology, dietician consult

reasons CKD pts admitted

1. cardiovasc (*uremic pericarditis, HTN, CHFe, dysrhyth.)

2. GU - stones, stenosis, inflam.

3. GI - bleed, stomatitis, N/V

4. endocrine, nutritional, metabolic

5. resp - resp failure d/t metabolic acidosis, pulm edema, uremic pleuritis/pneumonitis

KUSSMAUL

rapid, deep, labored breathing

K: ketones

U: uremia

S: sepsis

S: salicylates

M: methanol

A: aldehydes

U

L: lactic acid/osis

azotemia

-XS urea and nitrogenous substances in the blood

kidneys & acid-base balance

-DCT: secretes K+, H+, ammonia, reabsorbs HCO3-

-CKD & AKI have risk for metabolic acidosis

peritoneal dialysis vs HD

PD: lining of the peritoneal cavity = filter to remove waste from the blood

-preserves kidney fnctn better, gentler on body, no needles

HD: removes and filters blood then returns it

-risk for hypoTN

HD fistula

-joining of artery & vein in forearm

-cannot be used until fully healed (++ mos), large bruit = normal

-*vasc emergency if blood flow issues*

early signs of AKI

-oliguria initially (<400 ml in 24 hours)

-incr BUN and creatinine

RIFLE criteria

Risk: decr >25% of GFR OR serum Cr x1.5; decr UO <0.5mL/kg/hr x6H

Injury: Cr x2 or GFR >50%; <0.5mL/kg/h x12H

Failure: Cr x3 or GFR >75%; ?<0.5mL/kg/h x12H OR anuria x12H

Loss: irreversible AKI OR >4wks

ESRD: >3 mos

AKI

-sudden, often reversible reduction in kidney fnctn

-30% ICU admissions

Cr

-creatinine: indicator but not direct measurement

-breakdown of Cr PO4 2- from musc & protein metab

-released at constatn rate

-removed by kidneys via GFR & PCT secretion

-XY: 53-106mcmol/L

-XX: 44-97mcmol/L

GFR vs eGFR

-glomerular filtration rate; estimates kidney fnctn; normal 90-120mL/min

-eGFR: Estimated GFR is a calculated approx. of actual GFR

AKI risk factors

-chronic disease (i.e. CKD, HF, DM, LF, obesity)

-medication

-genes

pre-renal failure

-decr kidney perfusion = decr GFR

-i.e., (cardiac dysfnctn) MI, CHF; (vasodilation) sepsis, cirrhosis, anaphylaxis; (hypovolemia) hemorrhage, diuresis; (vasc resistance) surg., anesthesia

intra-renal failure (intrinsic)

-kidney damage from inflam or immunological processes or prolonged hypoperfusion

-acute tubular necrosis MOST common intra-renal

-i.e., glomerulonephritis, vasculitis, renal artery stenosis, renal vein thrombosis, ischemia, infxn, drugs

acute tubular necrosis: initiation & s/s

-damage to tubular epithelium from toxins, ischemia, sepsis

-incr Cr, BUN

acute tubular necrosis: maintenance & s/s

2. maintenance phase (oliguria)

-incr Cr, BUN; decr eGFR, CrCl

-oliguria, metab acidosis, N, fluid XS, anemia,

-incr PO4-, K+; decr Ca2+, Na+; uremia -> neuro changes

acute tubular necrosis: recovery & s/s

3. recovery phase

-renal tissue repair occurs, diuresis can start before renal function has fully returned

-incr eGFR; decr BUN, Cr

-1.5L UO/day

-hypovolemia, hypoT, dehydration, decr Na+ & K+

post-renal failure

Urine can't get out of the kidney

-i.e., urolithiasis, prostatic hypertrophy

modifiable cancer risk factors

-exposure to carcinogens & promoters

-diet high in processed food, red meat

-ETOH, smoking

-high BMI

-less than 30mins activity 5x/wk

breast CA risk factors

-1st degree relative w/ CA, BRCA1&2, HER2

-XX

->50yrs

-menopause HRT

-obese (BMI 18-25)

-early merache, late menopause

->35yrs at first pregnancy

phases of cancer development

1. Initiation: virus, hormone, radiation, genes etc. reach target cell & cause dysfnctn to cell division

2. Promotion: dysfcntl cell proliferates (now "cancer" cell)

3. Progression: evidence of disease; can lead to metastasis

neoplasia vs hyperplasia

N: uncontrollable, irreversible cell growth -> neoplasm; abnormal growth

H: reversible incr in cells from a stimulus; normal form of growth

immune system & cancer

-CA cells: tumour-associated antigens (TAA) spotted by Cytotoxic T cells -> cytokine release (interleukin, -feron)

-T cells, NK cells, macrophages, B cells come to site

B cells & CA

-b cells -> plasma cells & prod antibodies that attach to TAA & destroy cell

naming of CA

-benign: group of abnormal cells, grow slow, usually no Tx (unless obstructing)

-malignant: rapid growth, angiogenesis, expel cell contents, invade lymph/blood (metastasis)

grading of CA (histology)

-grade I mild dysplasia

-grade II mod. dysplasia

-grade III severe dysplasia

-anaplasia: IRREVERSIBLE, undifferentiated (no semblance to surrounding tissue/cells)

staging of CA (TNM)

T: tumour (To not found, Tis: in-situ, T1-4 size, Tx cannot measure)

N: nodes (No none nearby, N1-3 # of nodes, Nx unknown)

M: metastasis (Mo no spread, M1 spread, Mx cannot measure spread)

types of CA complications (2)

1. obstructive: SVC syndrome, spinal cord compression

2. metabolic: hypercalcemia, SIADH,

SVC syndrome (type, def'n, s/s, Tx)

-obstructive CA complic.

-tumour compresses SVC

-s/s: face edema, neck/chest vein distension, HA, seizures

-Tx: lift HOB, O2, steroids, radiation, chemo, stunting, thrombolysis, Sx

spinal cord compression (type, def'n, s/s, Tx)

-obstructive CA complic.

-tumour compresses SC

-s/s: localized pain, motor weakness, sensory paresthesia, loss/change to bowels & bladder

Tx: Sx, radiation

hypercalcemia (type, def'n, s/s, Tx)

-metabolic CA complic.

-osteolysis by osteoclasts from PTH protein that CA cells produce

-decr Ca+2 excretion, incr Ca+2 absorp., incr Ca+2 release in bones

Tx: phosphates, calcitonin, IV fluid, duretics

SIADH (type, def'n, s/s, Tx)

-metabolic CA complic.

-ADH released by CA cells, kidneys hold H2O

-s/s: hyponatremia, wt gain, weakness, anorexia, seizures, coma

-Tx: fluid restriction, CA treatment/removal

CA Tx: radiation

-ionization/excitation of particles and break DNA bonds

-damage occurs to both CA and non-CA cells but can recover usually

-goal: destroy or reduce tumour

CA Tx: brachytherapy

-insertion of radioactive seeds into cavity/tissue via needle

-HIGH dose of radiation - TAKE precs.

CA Tx: chemo

-standard Tx

-IVADs; interferes, mods, breaks down DNA or mods RNA tscription -> cell DEATH; done in cycles to help recoup normal cells/immune system

-goal: decr # of cells in primary & metastatic tumours; cure or palliation

nadir (chemo)

-lowest # of WBCs post-chemo

CA treatment complics (1)

-tumour lysis syndrome

-when large tumours treated w/ chemo, large cell debris spill into b stream (d/t cell necrosis)

-s/s: incr PO4-2, K+, uric acid (-> AKI risk); hypocalcemia

-Tx: IV fluids, phosphate binders, Ca2+ gluconate, diuretics, allopurinol (decr uric acid)