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MC II > week 1 > Flashcards

week 1 Flashcards

1
Q

kidney infection signs and symptoms

A
  • delirium
  • flu-like
  • LBP
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2
Q

functions of the renal system

A
  • filters waste products from metabolism (ammonia, drugs) - along with liver
  • regulates ion levels in plasm - K+ goes up with kidney issues
  • regulates blood pH - produces bicarb
  • conserves valuable nutrients - reabsorbs glucose
  • regulates blood volume - water balance
  • regulates RBC production - produces erythropoietin
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3
Q

kidneys make up _ body mass but receives _ % of cardiac output

A
  • 1% of body mass
  • 25% of cardiac output

kidneys have increased metabolic rate and so need increased O2 to maintain function

1.2-1.3 L/min in adult

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4
Q

anatomy of kidneys

A
  • paired, retroperitoneal: nearby structures inflamed with inflamed kidneys (LBP)
  • right lower than left
  • bean-shaped
  • concave surface - renal hilum, contains entry/exit of renal a/v and ureter
  • divided into outer cortex and inner medulla
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5
Q

renal cortex

A
  • outer portion of kidney
  • contains glomeruli and proximal/distal tubules
  • 75% of renal parenchyma is cortex
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6
Q

renal medulla

A
  • inner portion of kidney
  • cone-shaped - cones KA “renal pyramids”
  • 8-18 pyramids per kidney
  • contain Loops of Henle and collecting ducts
  • medullary pyramids narrow to renal papilla to emtpy urin/filtrate -> minor calyx -> major calyx -> renal pelvis -> ureter
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7
Q

functional unit of kidney is

A

nephron
* glomeruli and loop of henle
* each kidney has 1 million nephrons
* located in both cortex and medullary areas

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8
Q

glomerulus - tuft of capillaries

A
  • filters H2O, K+, sugar, salt -> everything but RBC
  • filtrate enters nephron, urine building block
  • surrounded by capillary network: exchange, ion/H2O/pH balance
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9
Q

_ % of filatrate automatically reabsorbed at proximal convoluted tubule

A

90%
* 10% to Loop of Henle: fine-tuning, reabsorb/conserve based on blood values, specizlied cells for transport (can be impacted by diuretics)

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10
Q

functions of nephron

A
  1. filtration: blood filtered in glomerulus -> tubule
  2. tubular reabsorption: solutes and H2O from lumen into peritubular capillaries and returned to circulation
  3. tubular secretion: filtrate in tubule further modified by secretion of substances (urea, meds) from peritubular capillaries into lumen
  4. urinary excretion: filtrate/urine is transported to bladder
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11
Q

normal urine output is _ with normal intake of _

A
  • output is 800-2,000 mL/day
  • intake is 2 L/day

euvolumia

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12
Q

different urine colors

A
  • normal: pale yellow
  • darker: more concentrated, dehydrated
  • pink to dark red: hematuria (RBC) in urine
  • cloudy: infection or WBC
  • rust: rabdo
  • also
  • polyuria: > 3L/day urine production, more dilute, in DM, decreased total blood volume
  • urinary frequency: urinate many times but normal or less than normal volume
  • nocturia: excessive urination at night
  • oligaria: daily urine output < 400 mL, indicative of increased mortality
  • anuria: no urine, ominous finding
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13
Q

prerenal causes of acute renal failure

A
  • heart failure
  • lack of perfusion
  • shock/sepsis
  • hemorrhage
  • hypovolemia
  • excess vomiting, diarrhea
  • diuretics
  • conditions that decrease renal blood flow (RBF)

55%

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14
Q

intrinsic/intra-renal causes of acute renal failure

A
  • kidney disease secondary to DM
  • high BP
  • kidney stones
  • interstitial nephritis, acute glomerulitis, tubular necrosis, ischemia, toxins
  • injury/inflammation of kidneys

40%

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15
Q

post-renal causes of acute renal

A
  • kidney stones in ureter
  • blood clot
  • bladder cancer
  • prostate/cervical cancer
  • conditions that obstruct urine outflow

5-15%

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16
Q

acute kidney injury (AKI)

A
  • severe UTI
  • infection
  • pyelonephritis: when a UTI goes to kidney and ureters
  • S&S: back pain, fever, chills, malaise, N/V, confusion, hematuria, painful urination

do Murphy’s percussion

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17
Q

intra/post renal caliculi/stones

A
  • increased [] of salts in blood: calcium salts, uric acid
  • UTI
  • urinary tract obstruction
  • S&S: N/V, renal/colic pain, hematuria
  • treatment: manage pain, hydration, cystoscope (snare and remove), lithotripsy (ultrasound)
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18
Q

rhabdomyolysis

A
  • breakdown of muscle fibers (sarcolemma): results in myoglobin release and waste into blood stream
  • myoglobin can cause AKI and ultimately renal failure
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19
Q

signs and symptoms of rhabdo

A
  • triad: muscle pain, weakness, dark urine
  • compartment syndrome due to inflammation and fluid shifts
  • AKI: increased myoglobin forms casts in nephron, iron degradation causes increase ROS
  • decreased urine output, reddish brown urine
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20
Q

rhabdo lab results

A
  • creatine kinase >5x ULN (normal is 60-174, 1500-100,000)
  • increased CK increases risk of AKI and kidney damage
  • hypovolemia due to ECF influx to muscles
  • hyperkalemia and hyperphosphatemia due to damaged muscle cells
  • hypocalcemia due to influx to injured muscles
  • metabolic acidosis due to kidney injury
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21
Q

causes of chronic renal failure (CRF)

A
  • diabetic neuropathy (>30%)
  • hypertension (20-25%)
  • glomerulonephritis (10%)
  • polycystic kidney disease (5%)
  • kidney infections, obstructions, renal vascular disease
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22
Q

stages of CKD

A
  • higher GFR is healthier kidney
  • early disease is “silent” but still damaging
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23
Q

assessment of renal function

A
  • glomerular filtration rate (GFR)
  • albumin
  • creatinine
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24
Q

GFR for renal function

A
  • flow rate of filtered blood through kidney over time
  • gives rough measure of number of functioning nephrons
  • difficult to measure: requires 24 hour urine collection and special dyes
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25
Q

albumin for renal function

A
  • albumin is protein made my liver, found in blood and not in urine
  • normal albumin in urine is zero?
  • more than 30 mg/g is albuminuria/proteinuria
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26
Q

creatinine for kidney function

A
  • not filtered if kidney is damaged
  • filtered in glomerulus and excreted by kidney (not reabsorbed)
  • as plasma C increases, GFR exponentially decreases
  • increased creatine in blood is decreased kidney function

most common test

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27
Q

potassium (K+) in renal dysfunction

A
  • hyperkalemia
  • muscle weakness, flaccid paralysis, paresthesias, ECG, widening of QRS progressing to ventricular tachycardia/fibrillation, cardiac arrest
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28
Q

calcium is renal dysfunction

A
  • hypercalcemia
  • stones (renal/biliary)
  • bones (pain)
  • groans (abdominal pain)
  • thrones (polyuria)
  • N/V, fatigue, ECG changes short QT interval
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29
Q

bicarbonate in renal dysfunction

A
  • metabolic acidosis (decreased HCO-3)
  • lethargy, fatigue, muscle weakness, decreased cardiac contractility, decreased cardiac output, dysrhythmias
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30
Q

peritoneal dialysis (PD)

A
  • uses peritoneum as semipermeable membrane and dialysate infused directly into abdomen
  • peritoneam highly vascularized: allows waste products and fluids to pass from blood to dialysis solution
  • dialysate infused into abdomen and allowed to remain for several hours prior to drainage
  • PT during infusion/removal
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31
Q

hemodialysis (HD)

A
  • attempts to perform normal kidney function by passing blood through semi-permeable membrane (dialyzer) allowing metabolic waste products to diffuse into a correction fluid (dialysate) - individual for patient
  • promotes correction of fluid and electrolyte abnormalities, toxic material removal, maintenance of acid-base balance
  • accomplished through vascular access that allows high flows and repeated cannulation while minimizing infection and clot formation

1 L/hr

32
Q

types of HD access

A
  • temporary access: tuneled catheter
  • in central vein (internal jugular), least durable
  • AV fistula: has “thrill”
  • surgeon constructs access by combining A and V
  • 3-6 months to mature but very durable
  • AV graft: man-made tube (gortex) inserted by surgeon to connect A and V
  • 2-6 weeks to mature, less durable than AV fistula
  • no BP measurement on arm with fistula
  • protect arm from injury
  • control hemorrhage: bleeding is arterial, maintain direct pressure
  • thrill is normal
33
Q

continuous renal replacement therapy (CRRT)

24/7 dialysis in ICU

A
  • if worried for CV status, low and slow - patients usually critically ill (hemodynamic status concern)
  • use extracorporeal blood circuit through small-volume, low-resistance filter
  • provider. continuous removal of solutes and fluid
  • PT may be contraindicated

100 mL/day

34
Q

implications of dialysis

A
  • mobilization activities are typically contraindiciated during HD and during inflow/outflow of dialysate with PD
  • CRRT may be an exception but need to know “hemodynamic stability”
  • assess fluid and electrolyte status
  • expect potential dehydration/hypovolemia, hypotension, and patient complaints of fatigue after
  • PD: dialysate in abdomen may cause SOB/DOE
  • mointor vitals closely
35
Q

functions of GI tract

A
  • digestion: physical breakdown, chemical alteration of food stuff to allow absorption along GI tract
  • involves GI motility, pH changes, biological detergents, enzymes
  • absorption: directed movement of nutrients across intestinal lining
  • excretion: food residue, hyrdophobic molecules (drugs, bacteria, dead cells)
  • host defense: largest lymphoid organ in body with extensive surface area
  • gut microbiome, implications in health
36
Q

esophagus

A
  • fibromuscular tube connecting throat/pharynx with the stomach (25 cm, < 1 in diameter)
  • food passes by peristaltic contractions
  • sphincters: bundles of muscle that control entry/exit (upper esophageal spincter - swallowing, lower - to stomach)

GERD

37
Q

gastroesophageal reflux disease

GERD

A
  • reflux of gastric contents (acid, pepsin, bile) into esophagus
  • contributing factors:
  • incompetent lower esophageal sphincter (LES)
  • impaired gastric emptying through pyloric sphincter to duodenum
  • hiatal hernia
  • alcohol abuse
  • more common in children with developmental delays
  • common in DM: CN X (vagus) damage
38
Q

complications of GERD

A
  • regurgitation/malnutrition
  • esophagitis
  • Barrett’s esophagus: pre-cursor to esophageal canacer (transformation of normal esophageal squamous epithelium to columnar epithelium) - pre malignant, increase risk for developing esophageal cancer
  • respiratory compromise, associated with asthma and COPD
39
Q

stomach

A
  • reservoir function: controlled release of chume into SI, stomach can expand to hold 2-4 L of fluid/food
  • mechanical digestion: gastric motility (peristalsis)
  • chemical digestion: digestive enzymes continue digestion of protein (pepsin), fats (lipase) –> lots of cells secrete mucus lining, protect against HCl
  • hydrochloric acid: chemical digestion, activates some digestive enzymes (pepsin), immune defence (kills bacteria)
  • intrinsic factor (IF) protein: bind vitamin B12 for absorption in SI (ileum) –> dysfunction is pernicious anemia

PUD, GIB

40
Q

gastric defense/mucosal defense

A
  • protective barrier/function
  • compact epithelial cell lining
  • mucus covering
  • bicarbonate ions (HCO-3): buffers H+
  • blood flow
41
Q

gastritis and peptic ulcer disease (PUD)

A
  • gastritis: inflammation of inner lining of stomach (mucosa)
  • acute: excessive acid production > gastric defense (NSAIDS, ASA, ETOH)
  • stress induced: common in critical illness, especially patients with mechanical ventilation
  • peptic ulcer disease: increased acid secretions and digestive enzymes erode digestive mucosa, H. pylori infection (>70%)
  • complications: hermorrhage, perforation peritonitis, scarring
  • defined by site of origin: gastric, duodenal, esophageal
42
Q

gastrointestinal bleeding (GIB)

A
  • check lab values: hemoglobin, hematocrit
  • 75% GI bleeding in upper tract: esophagus, stomach, small bowel
  • 20-25% in lower tract: terminal ileum, colon, rectum
  • 50% due to NSAID use: eldery, female
  • continued bleeding and re-bleeding are high predictors of mortality and morbidity in older patients
43
Q

GIB red flags

A
  • red flags: suggest shock
  • syncope, hypotension, pallow, diaphoresis, tachycardia
  • fatigue, weakness, SOB, abdominal discomfort
  • decrease in H/H
  • vomiting of blood (hematemesis): coffee ground emesis usually from upper GI bleed
  • black tarry stool (melena): can be U/LGIB
44
Q

NSAIDs

A
  • acetylsalicylic acid (ASA, aspirin, Bayer, Ecotrin)
  • traditional NSAIDs (ibuprofen, naproxen)
  • COX 2 inhibitors (Celebrex Viox)
45
Q

NSAIDs and GIB

A
  • 15% of long-term NSAIDs users develop PUD
  • ASA and traditionals block COX 1 and COX2: pain relief with increased GIB risk
  • celebrex and Vioxx are selective for COX 2 only: pain relef with decreased GIB risk but increase CVA/MI risk
  • COX 1 facilitates clotting
  • COX 1/COX 2 facilitate pain
  • blocking Cox 2 increases Cox 1 activity –> increased clotting, CVA/MI
46
Q

small intestine

absorbs nutrients

A
  • starts at pylorus and ends at ileocecal junction
  • 3 regions (proximal to distal): duodenum, jejunum, ileum
  • functions: mixes/grinds (segmentation) and propels (peristalsis) contents - coordinated, enteric NS
  • digests and absorbs nutrients
  • secrete regulatory hormones
47
Q

SI function

A
  • chemical digestion:
  • endocrine (hormone) cells and exocrine (digestive enzymes) function
  • food -> duodenum (endocrine) -> pancreas (exocrine)
  • hormones regulate gastric, pancreatic, and gall bladder function
  • chyme enters duodenum and releases cholescystokinin (CCK) that increases pancreatic enzyme and bile release
  • absorption:
  • villi and micromilli: increase intestinal absorptives - absorption of nutrients
  • lacteals (lymphatic capillaries) for fat absorption (chyle)
48
Q

large intestine

water balance

A
  • function
  • final stage of digestion through bacterial action: ferment carbs, produce B vitamines, vitamin K
  • mucus is major secretion: no enzyme secretion
  • main role of colon is re-absoprtion of water with ions and vitamins: epithelial cells reabsorb salts, water flows by osmosis

CD, UC, IBS, celiac, acute, CA

49
Q

crohn’s disease and ulcerative colitis

A
  • CD: patchy inflammation that may occur anywhere along digestive tract (entire bowel wall)
  • pain is commonly experienced in right lower abdomen
  • UC: inflmmation continuous throughout affected LI/colon
  • innermost lining/mucosa
  • pain is common in lower left abdomen
  • common presentation
  • abdominal cramping/pain, diarrhea, obstruction, fatigue, malabsorption (weight loss/malnutrition)
  • joint pain, anemia
  • medical management
  • immunosuppressants: azathioprine
  • biologics: infliximab, adalimumab (TNF alpha R blocker)
  • anti-inflammatory agents: steroids
  • surgery: surgical resection of bowel, especially in Crohn’s
50
Q

irritable bowel syndrome (IBS)

A
  • disturbed bowel function without structural abnormalities
  • spasmodic motility pattern
  • malabsorption
  • nutrition deficiency and loose stools
  • etiology unknown but believed to be related to Colonic sensitivity
  • diagnosis of exclusion: exclude UC, CD, diverticulosis
51
Q

Celiac disease

A
  • autoimmune disorder that occurs in genetically predisposed
  • ingestion of gluten leads to SI damage
  • leads to malabsorption and symptoms of bloating, diarrhea, gas, fatigue
  • other issues: anemia (decreased absoprtion of Fe, B12), osteoporosis (decrease absorbed Ca, vD)
52
Q

hernia

A
  • protrusion of organ through wall of cavity that normally contains it
  • hiatal: gastro-esophageal junction moves above diaphragm with some stomach
  • ventral: incision-related hernia where abdomen contents protrude throug linea alba
  • inguinal: protrusion of abdominal cavity through inguinal canal
53
Q

acute abdomen

A
  • KA peritonitis
  • sudden, sever abdominal pain < 24 hours
  • often a medical emergency
  • causes: appendicits, cholecystitis, pancreatitis, ischemic bowel, AAA
  • physical exam: identify location, palpation reveals rigidity/rebound tenderness, bowel sounds diminished/absent
54
Q

colorectal cancers

A
  • progression often starts with benign polyp (early detection in colonoscopy)
  • symptoms: bleeding, pressure/pain with defecation, change in elimination
  • associated with age, family history, diet, exercise, UC/CD
  • 3rd most common CA and 3rd leading cause of death
55
Q

ileectomy

A

resection of SI

56
Q

colectomy

A

resection of large intestine

57
Q

ostomy

A

surgically created opening in body for discharge of body wastes

ileostomy: SI
colostomy: large bowel

58
Q

stoma

A

end of SI or LI that is protruding through abdominal wall

59
Q

benefits of bariatric surgical procedures

A
  • weight loss
  • remission of T2 diabetes
  • improvement in CV risk factors and CV health: improved lipid profiles, decreased BP or HTN
  • improvements in mental health: decreased depression
  • better sleep: decreased obstructive sleep apnea
  • decreased hip and knee pain
  • improved fertility
60
Q

additional considerations for bariatric surgical procedures - GI disorders

A
  • absorptive disorders (IBS, UC, Crohn’s)
  • nutrition deficiencies - malnutrition
  • post-op pulmonary complications: increased risk with upper > lower abdominal surgery
61
Q

common post-op complications (POC) with bariatric surgery

A
  • pain, bleeding, infection, post-surgery adhesions
  • pulmonary complication: atelectasis, desat, PNE, PE, respiratory failure
  • ileus: partial, paroxysmal - decreased motility, paraylsis of bowel, leads to constipation/discomfort/NV
  • bowel leakage: sepsis
62
Q

medications for GI

A
  • antacids: drugs that decrease acid secretion by gastric parietal cells
  • proton pump inhibitors: prilosec, nexium, prevacil
  • H2 receptor blockers: pepcid
63
Q

pancreas

A
  • endocrine and exocrine function
  • endocrine: islets of Langerhands - hormones, insulin, glucagon
  • exocrine: duct cells secrete NaHCO3, acinar cells secrete digestive enzymes -> exocrine portion of pancreas are acinar and ducts
64
Q

pacreatitis

A
  • inflammation of pancreas
  • acute: NV, fever
  • chronic: low flying, masks as MSK/LBP
  • pancreatic enzymes (especially trypsin) activated in pancreas instead in SI – leads to inflammation and autodigestion
  • 80,000 cases per year: 90% from alcohol abuse or gall stones
  • severe abdominal/epigastric pain - radiates to back, NV, worse after fatty foods, relieved with forward leaning
  • dehydration –> hypotension
  • severe pain leads to HTN and tachycardia
65
Q

pancreatic insufficiency and cystic fibrosis

A
  • enzyme synthesis and secretion normal
  • inability to secrete bicarb and water: limits amount of enzymes released to intestinal lumen
  • if they reach lumen, often inactive: not enough alkaline to neutralize gastric acid
  • treatment: enzyme supplements and antacids
66
Q

liver anatomy

A
  • consists of 2 main lobes, both made of 8 segments: each segment made of thousands of lobules
  • circulation includes: hepatic a (20-40%) - O2 enriched blood, portal v (60-80%) nutrient enriched blood, hepatic v
  • in RUQ
  • percussion dullness in mid clavicular line used to determine liver span
  • upper border: 5-7th intercostal space
  • lower border: usually ends at costal border
67
Q

liver functions

A
  • excretory: production of bile for digestion of fats
  • sympathetic: produces plasma proteins (albumin) and coagulation factors, synthesizes triglycerides/cholesterol/carbs
  • metabolism: storage site for glycogen/gluconeogensis (glucose storage), protein catabolism and synthesis of urea, breaks down RBCs and remove excess bilirubin
  • detoxification: detoxifies noxious compounds found in chemicals (ETOH) and drugs (first pass effects)
68
Q

with liver problems

A
  • decreased albumin production/in blood –> decreased water reabsorption
  • fluid in blood slowly decreases
  • look swollen (ascites) –> BUT patient is hypovasculate (low BP)
  • do not use diuretics to get rid of fluid
69
Q

S&S of hepatic dysfunction

A
  • jaundice: excessive deposition of bile pigments (hyperbilirubinemia, >1.3 mg/dL)
  • ascites: abdominal swelling/fluid in peritoneum, leakage from portal v system
  • due to portal HTN and/or hypoalbuminemia
  • develops due to: altered starling forces in portal vv (low oncotic pressure due to hypoalbuminemia), with increased portal venous pressure
  • medical interventions: diuresis and Na restriction, paracentesis (fluid removal from abdominal cavity)
70
Q

hepatic disorders – pulmonary complications

A
  • ascites can impact diaphragm and lung volumes: fluid volume elevates diaphragm –> decreased lung volume, rapid/shallow breathing, looks like restrictive lung pathology
  • hepatopulmonary syndrome: watch out or O2 desat
71
Q

varices

A
  • portal HTN causes congestion in spleen, stomach, esophagus
  • collateral vessels develop which become distneded and varicose (stomach and esophagus)
  • varices may burst, leading to upper GI bleeding/hematemesi
72
Q

hepatic encephalopathy

A
  • reversible decrease in neurologic function due to shunting of blood awy from portal circulation
  • associated with hepatic failure resulting in accumuluation of noxious metabolic by-products, most commonly associated with increased serum ammonia
  • S&S: asterixis (liver flap) - alternating flexion/extension of hands when patient asked to extend wrist with arms extended
73
Q

aneurysm

A

ballooning and weakening of vessel wall

74
Q

dissection

A

tear in intimal layer

75
Q

presentation of ruptured/dissection AAA

abdominal aortic aneurysm

A
  • sudden abdominal/back pain - tearing sensation
  • hypotension and tachycardia: sweating, clamminess, dizziness
  • NV
  • pulsatile mass in abdomen (obscured by obesity) - if < 5 cm, not detected usually

hypoTN: losing blood into walls of aorta - eventually everything bursts

76
Q

aneurysm risk factors/complications

A
  • RF: age, family history, HTN, high cholesterol, CAD/atherosclerosis, smoking, male
  • complciations: thrombosis, distal emoblization, dissection and rupture

do not go over 90 bpm, 150 systolic

MC II (7 decks)

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