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312 Patho > EXAM 5 > Flashcards

EXAM 5 Flashcards

1
Q

MOTILITY

A

movement of food through the body from mouth to anus

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2
Q

peristalsis

A

involuntary contractions of the intestinal muscles that create wave
movements to propel substances forward

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3
Q

sphincter

A

Ring of muscle that closes an opening like at the stomach

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4
Q

mastication

A

chewing

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5
Q

enteric

A

occuring in the intestines

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6
Q

chyme

A

Acidic fluid that moves from the stomach to the small intestine. Consists of gastric juices and partly digested food

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7
Q

defacation

A

Discharge of feces from the body

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8
Q

intestinal flora

A

Naturally occurring bacteria in the intestine

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9
Q

digestion

A

Process of breaking down food into what the body can use and needs

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10
Q

Absorption

A

Action of one thing taking up or being taken up by another

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11
Q

describe the anatomy of the upper gi tract

A
  • 4 layer structure, oral cavity, salivary glands, esophagus, stomach, small intestines- digests food and gets it ready for processing as well as digestion.
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12
Q

describe the anatomy of the middle gi tract

A

lower duodenum, 2/3 of transverse colon- processes food that small intestine couldn’t by absorbing minerals and water

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13
Q

describe the anatomy of the lower gi tract

A

last 1/3 of transverse colon, upper part of the anal canal- dehydrates and stores fecal material

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14
Q

what are the anatomical landmarks of the stomach

A

cardia, fundus, body, pylorus

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15
Q

cardia

A

surrounds superior opening,

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16
Q

fundus-

A

rounded, gas filled portion superior and left of the cardia,

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17
Q

body-

A

large part beneath the fundus.

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18
Q

Pylorus-

A

area connecting to the duodenum

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19
Q

Saliva-

A

starts digestion, helps chew and swallow, protects teeth,

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20
Q

gastric juice-

A

acidic fluid in stomach that promotes digestion,

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21
Q

bile-

A

bitter and alkaline fluid that is secreted by the liver and aids digestion,

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22
Q

pancreatic fluid-

A

alkaline (bicarbonate)- critical for digestion of protein, fats, and carbs

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23
Q

What is the function of the peritoneum?

A

Membrane of smooth tissue that pads and insulates organs and holds them in place. It secretes fluid to reduce friction when organs rub against each other.

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24
Q

passage of food through the gi tract

A

Food goes into mouth masticationswallowesophaguslower esophageal sphincterstomachpyloric sphincterenters small intestine small intestine  duodenum  jejunum ileum ileocecal valve  enters large intestine cecum  ascending colon transverse colon  descending colon  rectum  internal anal sphincter external anal sphincter

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25
Q
  1. What are the hormones of the GI tract?
A

CHOLECYSTOKININ, SECRETIN (GLP-1 AND GIP), GASTRIN, GHRELIN

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26
Q

Discuss intestinal flora and the role in digestion and absorption.

A

Intestinal flora helps supply nutrients, process vitamins and digest cellulose. They have a direct affect on mineral absorption.

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27
Q
  1. Is the gut of a normal adult sterile?
A

no

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28
Q
  1. Where is the largest ecosystem of microbes in the GI tract found?
A

Large intestine followed by the small intestine

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29
Q
  1. What role do microorganisms play in the GI tract?
A

They aid the immune system and ensure the integrity of the mucosal lining.

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30
Q
  1. What might cause a disruption of intestinal flora and lead to opportunistic infection?
A

Diet, antibiotics or other meds, or other environmental factors

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31
Q
  1. Name the three sections of the small intestine.
A

Duodenum, jejunum, and ileum

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32
Q
  1. What is the action of pepsin?
A

Breaks down proteins into peptides and amino acids to be absorbed in the small intestine.

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33
Q
  1. What is the name of the sphincter located between the stomach and the small intestine?
A

Pyloric sphincter

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34
Q
  1. What type of acid-base problem would you anticipate having if you have had frequent prolonged vomiting?
A

Metabolic alkalosis

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35
Q
  1. What layer of the GI tract contains blood vessels, nerves, and structures responsible for secretion of digestive enzymes?
A

submucosa

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36
Q
  1. What structure covers the larynx and prevents aspiration when swallowing?
A

epiglottis

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37
Q
  1. In what part of the GI tract does the majority of nutrient absorption occur?
A

small intestine

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38
Q
  1. Does everyone who has gastroesophageal reflux have GERD?
A

no

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39
Q
  1. Is there an association between GERD and asthma?
A

yes

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40
Q
  1. Why would sitting up help to relieve the symptoms of GERD?
A

It allows gravity to work to keep contents down when the muscle is too weak and allows backflow.

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41
Q
  1. What are the complications of GERD?
A

Esophagitis and barret’s esophagus, gi bleeding, ulcerations, narrowing esophagus

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42
Q

why does liver damage cause tarry stools

A

Liver damage has stopped blood from flowing through the portal vein correctly. This causes the bile to not be broken down as it should be.

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43
Q

what do the following symptoms suggest
multiple loose tarry stools, dizzy, rapid hr, weak, thirsty with a Hx of arthiritis treated with daily aleve, advil. pt also sometimes drinks beer and smokes to ease the pain.

A

There is damage at a cellular level because of what it takes to metabolize these ingested substances. At this point, the patient probably has cirrhosis in it’s late stages.

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44
Q

c. What are the two most common causes of peptic ulcer disease?

A

h. pylori and aspirin/nsaids  action of acid and pepsin

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45
Q
  1. What are some causes of mechanical bowel obstruction?
A

Adhesions, volvulus, incarcerated inguinal hernia, intussusception

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46
Q
  1. Why is a patient with C. difficile infection on contact precautions in the hospital?
A

C diff is airborne transmitted.

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47
Q
  1. List the functions of the liver.
A

SECRETION OF BILE, METABOLISM OF BILIRUBIN, VASCULAR/HEMATOLOGIC FUNCTION, METABOLISM OF NUTRIENTS, METABOLIC DETOXIFICATION, STORAGE OF MINERALS AND VITAMINS

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48
Q
  1. Why do patients develop jaundice?
A

Usually a sign of liver disease causing a buildup of bilirubin.

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49
Q
  1. Which blood tests monitor liver function?
A

Alt, ast, alp, ggt, pt, inr are the typical tests.

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50
Q
  1. Is liver damage in Cirrhosis reversible?
A

No, but it can be slowed down

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51
Q
  1. What are the complications of portal hypertension?
A

Bleeding in the esophagus and stomach, peritonitis, hepatorenal syndrome

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52
Q
  1. Compare and contrast cholelithiasis and cholecystitis.
A

Cholecystitis can be acute or chronic inflammation, usually from an obstruction. Cholelithiasis is gallstones, which are a buildup of cholesterol or bilirubin. Both are due to excessive bilirubin, but cholelithiasis is from bile composition rather than backup. Both are diagnoses with US or CT and both require surgery. Cholelithiasis can be asymptomatic until large enough to cause obstruction, jaundice, or biliary colic. Cholecystitis symptoms may range from RUQ pain, mild fever, n&v, elevated wbc and anorexia to gi discomfort, gallbladder enlargement, and intolerance to certain foods.

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53
Q

FUNCTION OF THE KIDNEYS

A

EXCRETORY AND ENDOCRINE FUNCTION

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54
Q

WHAT EXACTLY DO THE KIDNEYS REGULATE

A

WATER, ELECTROLYTES, AND ACID-BASE BALANCE

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55
Q

WHAT DO THE KIDNEYS EXCRETE

A

FOREIGN CHEMICALS AND METABOLIC WASTE MATERIALS

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56
Q

WHAT DO THE KIDNEYS SYNTHESIZE AND ACTIVATE

A

RENIN, ERYTHROPOIETIN, VITAMIN D, AND PROSTAGLANDINS

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57
Q

WHAT ORGANS STORE AND TRANSPORT URINE

A

URINES, BLADDER, URETHRA

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58
Q

WHAT CAN STIMULATE ERYTHROPOIETIN RELEASE FROM THE KIDNEYS

A

STATES OF DECREASED BLOOD OXYGENATION

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59
Q

WHAT IS ERYTHROPOEITIN (EPO)

A

HORMONE THAT STIMULATES STEM CELLS WITHIN OUR BONE MARROW TO INCREASE RBC PRODUCTION

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60
Q

NEPHRON

A

MAIN FUNCTIONAL UNIT OF THE KIDNEY

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61
Q

HOW MANY NEPHRONS DOES EACH KIDNEY HAVE

A

ABOUT 1.2 MILLION

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62
Q

WHAT HAPPENS TO NEPHRONS OVER TIME

A

THEY DO NOT REGENERATE
DECLINE WITH AGE

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63
Q

HOW FAST DOES THE NEPHRON COUNT DECLINE

A

10% PER DECADE BEGINNING AT AGE 40

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64
Q

WHY DO WE HAVE A VERY LARGE RENAL RESERVE

A

SO THAT OUR KIDNEYS ARE ABLE TO FILTER BLOOD AND FILTER OUT TOXINS, WASTE PRODUCTS, AND FLUIDS VERY EFFECTIVELY

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65
Q

HOW MANY NEPHRONS CAN WE LOSE BEFORE WE START SEEING ANY IMPAIRMENT

A

50%
BUT GENERALLY 75-90% OF NEPHRON LOSS BEFORE WE SEE SERIOUS IMPAIRMENT

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66
Q

GLOMERULUS

A

WHERE THE FILTRATION PRIMARILY OCCURS
MAIN PART THAT ACTUALLY FILTERS THE BLOOD

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67
Q

EXPLAIN THE OVERVIEW OF THE NEPHRON BEYOND THE GLOMERULUS

A

PRIMARILY TUBULAR COMPANENTS WHERE ELECTROLYTES AND OTHER SUBSTANCES THAT ARE NEEDED TO MAINTAIN OUR HOMEOSTASIS ARE REABSORBED BACK IN THE BLOODSTREAM

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68
Q

HOW ARE MATERIALS WE DON’T NEED IN THE BODY SECRETED

A

WITHIN OUR TUBULAR FILTRATE FOR ELIMINATION

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69
Q

NEPHRON FUNCTION

A
  1. FILTRATION
  2. REABSORPTION
  3. SECRETION
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70
Q

NEPHRON FILTRATION

A

OF WATER SOLUBLE SUBSTANCES FROM BLOOD

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71
Q

NEPHRON REABSORPTION

A

OF FILTERED NUTRIENTS, WATER, AND ELECTROLYTES

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72
Q

NEPHRON SECRETION

A

OF WASTES OR EXCESS SUBSTANCES INTO THE FILTRATE

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73
Q

DIFFERENT SEGMENTS OF THE NEPHRON SPECIALIZE TO ACCOMPLISH WHAT

A

ALL NEPHRON FUNCTIONS

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74
Q

GLOMERULUS LAYERS

A
  1. CAPILLARY ENDOTHELIUM
  2. BASEMENT MEMBRANCE
  3. OUTER CAPILLARY ENOTHELIUM PODOCYTES
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75
Q

WHAT DOES THE PROXIMAL TUBULE REABSORB

A

NA
CL
HCO2
K
H2O
GLUCOSE
AMINO ACIDS

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76
Q

WHAT DO THE PROXIMAL TUBULES SECRETE

A

H+
ORGANIC ACID AND BASES

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77
Q

WHAT DOES THE THIN DESCENDING LOOP OF HENLE REABSORB

A

H2O

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78
Q

WHAT DOES THE THICK ASCENDING LOOP OF HENLE REABSORB

A

NA
CL
K
CA
HCO2
MG

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79
Q

WHAT DOES THE THICK ASCENDING LOOP OF HENLE SECRETE

A

H

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80
Q

WHAT DOES THE EARLY DISTAL TUBULE REABSORB

A

NA
CL
CA
MG

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81
Q

WHAT DOES THE LATE DISTALE TUBULE AND COLLECTING DUCT INCLUDE

A

PRINCIPAL CELLS
INTERCALATED CELLS

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82
Q

WHAT DO PRINCIPAL CELLS REABSORB

A

NA
CL

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83
Q

WHAT DO PRINCIPAL CELLS SECRETE

A

K

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84
Q

WHAT ARE RESPOONSIBLE FOR ADH MEDIATED H2O REABSORPTION

A

PRINCIPAL CELLS

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85
Q

WHAT DO INTERCALATED CELLS REABSORB

A

HCO2
K

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86
Q

WHAT DO INTERCALATED CELLS SECRETE

A

H

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87
Q

DURING GLOMERULAR FILTRATION, WHAT MOVES FROM THE BLOOD THROUGH THE GLOMERULUS AND INTO THE BOWMAN’S CAPSULE

A

WATER AND SMALL SOLUTES
*LARGER MOLECULES, PROTEINS, AND BLOOD CELLS ARE UNABLE TO MOVE THROUGH

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88
Q

WHAT IS THE RESULTING FLUID OF GLOMERULAR FILTRATION CALLED

A

GLOMERULAR FILTRATE

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89
Q

GLOMERULAR FILTRATION RATE
GFR

A

125 mL OF GLOMERULAR FILTRATE PRODUCED PER MINUTE

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90
Q

HOW MUCH BLOOD PERFUSES THE KIDNEYS

A

20-25% OF NORMAL CARDIAC OUTPUT
(1000-1300 ML/MIN)
*PROMOTES GLOMERULAR FILTRATION

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91
Q

PRIMARY FILTRATION PRESSURES

A

GLOMERULAR BLOOD HYDROSTATIC PRESSURE
2-3X HIGHER THAN OTHER CAPILLARY BEDS IN THE BODY

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92
Q

WHAT HELPS MAINTAIN BLOOD FLOW AND GFR

A

INTRARENAL AND EXTRARENAL FEEDBACK MECHANISMS

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93
Q

Neural/Humoral Controls

Regulation of Renal Blood Flow -GFR

A

– Sympathetic stimulation
– Angiotensin II, ADH, prostaglandins

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94
Q

Renin angiotensin system

Regulation of Renal Blood Flow -GFR

A

Control of blood pressure

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95
Q

Autoregulation

Regulation of Renal Blood Flow -GFR

A

– Maintain blood flow to provide a constant GFR that allows for solute and water excretion
– Renal systems responds to arterial pressure changes and sodium chloride concentrations

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96
Q

INCREASED PROTEIN AND GLUCOSE LOADS

Regulation of Renal Blood Flow -GFR

A

Increase GFR

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97
Q

What is Glomerular filtration rate used to evaluate

A

renal tissue function

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98
Q

what does decrease in bp do to gfr

A

decreases hydrostatic pressure that drives filtration
decreases gfr

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99
Q

what does an increase in protein and glucose do to gfr

A

increase gfr

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100
Q

what does sympathetic nervous system activation do to gfr

A

decrease gfr

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101
Q

how do hormones like angiotensin II affect gfr

A

efferent arteriole vasoconstriction increases b/p –> increases gfr

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102
Q

how does age affect gfr

A

loss of nephrons –> decreased gfr

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103
Q

how does the presence of prostaglandins affect gfr

A

increase gfr

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104
Q

normal creatinine level

A

adult:
0.6-1.2 mg/dl

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105
Q

what is creatinine

A

non protein end product of skeletal muscle metabolism

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106
Q

to what degree is creatinine eliminated

A

to the degree renal function will allow

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106
Q

how does creatinine indicate renal function

A

most specific indicator of renal function- estimates function capacity of the kidney

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107
Q

normal bun level

A

8-20 mg/dl in adult

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108
Q

urea

A

byproduct of protein metabolism that is eliminated entirely by the kidney

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109
Q

what happens to urea as renal function declines

A

it accumulates

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110
Q

other than renal disease, what else can cause bun elevation

A

high protein diet
gi bleeding

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111
Q

Urinalysis –

A

gross and microscopic exam of urine to evaluate ph, specific gravity and presence of abnormal substances and formed elements

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112
Q
  • Gross exam –

urinalysis

A

color, clarity, odor, sediment

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113
Q
  • Microscopic

urinalysis

A

– RBC, WBC, epithelial cells, casts, crystals, bacteria, pH

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114
Q
  • Specific gravity

urinalysis

A

– concentration of solutes, hydration status, functional ability of kidney

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115
Q

normal specific gravity level in adults

A

(1.010-1.025)

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116
Q

Polyuria

A

– increased volume of urine voided

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117
Q
  • Oliguria
A

– urine output less than 400ml/day

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118
Q
  • Anuria
A

– urine output less than 50ml/day

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119
Q
  • Nocturia
A

– excessive urination at night

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120
Q
  • Hematuria
A

– red blood cells in the urine

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121
Q
  • Proteinuria
A

– abnormal amounts of protein inthe urine

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122
Q
  • Dysuria
A

– painful or difficult voiding

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123
Q

Frequency

A

– frequent voiding, more thanevery three hours

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124
Q
  • Urgency
A

– strong desire to void

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125
Q
  • Hesitancy
A

– delay, difficulty in initiating voiding

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126
Q
  • Enuresis
A

– involuntary voiding during sleep

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127
Q

What is the functional unit of the kidney called?

A

nephron

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128
Q

What structure in the nephron filters blood?

A

glomerulus

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129
Q

What forces drive glomerular filtration?

A

Capillary hydrostatic pressure (Pc) and Bowman’s space oncotic pressure (πi) favor filtration into the tubule, and Bowman’s space hydrostatic pressure (Pi) and capillary-oncotic pressure (πc) oppose filtration.

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130
Q

What lab test is the most specific indicator of renal function?

A

urinalysis

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131
Q

what age can obstructive renal disorders occur

A

at any age

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132
Q

where can obstructive renal disorders occur

A

any area of the renal system

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133
Q

what are common causes of obstructive renal disorders

A

– Developmental defects
– Pregnancy
– Benign prostatic hypertrophy
– Infection, inflammation
– Tumors – common cause
– Stones – common cause

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134
Q

what are the effects of obstructive renal disorders

A

urinary stasis –> infection/backpressure –> hydroureter, hydronephrosis

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135
Q

Hydronephrosis Pathophysiology

A

Complete obstruction -> hydronephrosis -> decreased GFR -> ischemia -> increased pressure -> kidney damage

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136
Q

Renal Calculi

A

Crystalline structures that form from components, normally excreted in urine

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137
Q

requirements for renal calculi formation

A

supersaturation
nucleus (nidus)
deficiency of inhibitors

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138
Q

why is supersaturation of crystaline structures required for renal calculi formation

A

supports continued crystallization of stone components

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139
Q

why is nucleus (nidus) required for renal calculi formation

A

for the crystal to form around

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140
Q

what inhibitors of stone formation will we se a deficiency of in renal calculi formation

A

magnesium
citrates

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140
Q

types of stones

A
  1. Calcium (oxalate, phosphate or combo) – most common
  2. Magnesium ammonium phosphate (struvite)
  3. Uric Acid (urate)
  4. Cystine
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140
Q

clinical manifestations of renal system calculi

A
  1. pain- renal colic or non colicky
  2. n&v
  3. cool, clammy skin
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141
Q

renal colic

renal calculi pain

A

(often ureteral) pain, acute, rhythmic progressively, intense, initiates in flank and can radiate.

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142
Q

Non-colicky

renal calculi pain

A

– pain dull, deep ache in flank, varies in intensity

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143
Q

diagnosis

Renal System Calculi

A

Clinical symptoms, history to include diet, meds, complicating factors
urinalysis
stone analysis
bun/cr
xray, ct, us, ivp, nuclear scintigraphy

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144
Q

what findings on a urinalysis indicate renal system calculi

A

hematuria, infection, presence of crystals, urine pH

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145
Q

treatment

Renal System Calculi

A

meds
stone removal
prevention of recurrence
diluting urine
diet
measures to change urine ph
meds to reduce stone causing substances

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146
Q

meds used for renal system calculi

A

pain meds, antiemetics, antibiotics for infections

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147
Q

lithotripsy

A

fragments of stone
urteroscopic removal

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148
Q

how do you dilute urine

A

decrease supersaturation with 2l fluids/day

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149
Q

uti

A

Infection of the urinary system

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150
Q

host defenses

uti

A

– Washout phenomenon – voiding
– Mucin lining of bladder – barrier protects against invasion of organisms
– Body’s immune defenses

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151
Q

– Washout phenomenon

A

– voiding to reduce/eliminate uti

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152
Q

– Mucin lining of bladder

A

– barrier protects against invasion of organisms

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153
Q

Pathogen virulence

uti

A

– Bacteria with pili or fimbriae – adhere
– Lipopolysaccarides – bind to host cells and ilicit inflammatory response
– Enzymes that break down RBC, make iron available for bacterial metabolism, multiplication

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154
Q

Lipopolysaccarides

uti

A

– bind to host cells and ilicit inflammatory response

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155
Q

entry

uti

A

ascending or bloodborne

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156
Q

Escherichia coli

uti

A

– common infecting organism, lower UTI

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157
Q

is upper or lower uti more serious

A

upper

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158
Q

CAUSES OF UTI

A

obstruction, reflux (vesicoureteral and urethrovesical), catheters

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159
Q

CLINICAL MANIFESTATIONS OF UTI

A

frequency, dysuria, lower back or abdominal discomfort, chills, fever

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160
Q

DIAGNOSIS OF UTI

A

H&P, ultrasound, CT, renal scans to identify contributing factors, urinalysis, urine culture

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161
Q

TREATMENT OF UTI

A

location of infection, pathogen causing, acute, chronic or recurrent infection, antibiotics, increased fluid intake

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162
Q

Vesicoureteral reflux

A

– abnormal backflow of urine from the bladder into the ureter

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163
Q

Glomerulonephritis

A

– group of diseases that result in inflammation and/or injury to the glomerulus

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164
Q

What is the 2nd leading cause of kidney failure

A

Glomerular Disease

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165
Q

what happens in glomerular disease

A

Disruption of glomerular filtration and alteration of permeability of glomerular capillary membrane

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166
Q

is glomerular disease a primary or secondary condition

A

could be either

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167
Q

what are the triggers of glomerular disease

A

infectious microorganisms, immune mechanisms, environmental agents

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168
Q
  • Clinical manifestations of glomerular disease
A

nephritic or nephrotic syndrome.

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169
Q

Nephritic syndrome

A

– inflammatory response –> hematuria, red cell casts in urine, decreased GFR, azotemia, oliguria, hypertension

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170
Q
  • Nephrotic syndrome
A

– increased permeability of the glomerulus – massive proteinuria, hypoalbuminemia, generalized edema, lipiduria and hyperlipidemia

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171
Q
  • Asymptomatic
A

– hematuria, proteinuria aren’t recognized

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172
Q

BOWMAN’S CAPSULE

A

DOUBLE WALLED CAPSULE ENCASING THE GLOMERULUS

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173
Q

INNER CAPILLARY ENDOTHELIUM

A

INNERMOST STRUCTURE
SINGLE LAYER THICKNESS OF EPITHELIAL CELLS THAT REST ON THE BASEMENT MEMBRANE. THERE ARE A LOT OF SPACES BETWEEN THE CELLS

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174
Q

FINISHTRATIONS

A

SPACES BETWEEN ENDOTHELIAL CELLS OF INNER CAPILLARY ENDOTHELIUM WHERE SUBSTANCES CAN MOVE IN AND OUT

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175
Q

BASEMENT MEMBRANE

A

PREVENTS PLASMA PROTEINS, ERYTHROCYTES, LEUKOCYTES, PLATELETS ETC FROM PASSING THROUGH

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176
Q

OUTER CAPILLARY ENDOTHELIUM

A

SEPERATES THE BLOOD FROM THE CAPILLARIES OR IN THIS CASE FROM THE FILTRATE WITHIN THE BOWMAN’S CAPSULE

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177
Q

PODOCYTES

A

FOOT PROCESSES THAT SURROUND THE GLOMERULUS.

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178
Q

SLIP PORES

A

SPACES BETWEEN THE PODOCYTES

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179
Q

WHAT DO PODOCYTES DO

A

MAKE THE GLOMERULUS VERY PERMEABLE. MORE SO THAN ANY OTHER CAPILLARY

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180
Q

WHEN WE SEE GLOMERULUS ISSUES, SPECIFICALLY WITH THE PODOCYTES, WHAT DO WE OFTEN SEE

A

PROTEIN IN THE URINE
BLOOD CELLS IN THE URINE

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181
Q

TUBULAR REABSORPTION

A

REMOVAL OF MATERIALS FROM THE FILTRATE THAT’S BEEN DEVELOPED WITHIN THE GLOMERULUS

182
Q

TUBULAR SECRETION

A

FLUIDS AND SUBSTANCES THAT ARE ADDED TO THE FILTRATE AFTER IT HAS BEEN EXTRACTED FROM THE GLOMERULUS

183
Q

FILTRATION IS DRIVEN BY WHAT

A

HYDROSTATIC PRESSURE SO BLOOD CIRCULATES THROUGH THE CAPILLARIES, BLOOD IS PUSHED AGAINST THE WALLS AND FLUID IS FILTERED OUT

184
Q

HOW DOES STIMULATION OF THE SYMPATHETIC NERVOUS SYSTEM REGULATE GFR

A

HR INCREASE –> BP INCREASE –> INCREASED CARDIAC OUTPUT –> INCREASE SUPPLY OF BLOOD FLOW TO THE KIDNEY

185
Q

HOW DOES ANGIOTENSIN II AFFECT GFR

A

STIMULATES THE RELEASE OF ALDOSTERONE IN THE KIDNEYS TO INCREASE BP AND THUS INCREASE BLOOD VOLUME

186
Q

HOW DOES ADH AFFECT GFR

A

MAKES US HOLD ON TO OUR FLUID WHICH INCREASES CIRCULATING BLOOD VOLUME

187
Q

HOW DO PROSTAGLANDINS AFFECT GFR

A

DILATING EFFECT INCREASES RENAL BLOOD FLOW AND THUS GFR

188
Q

HOW DOES THE RENIN ANGIOTENSIN SYSTEM AFFECT GFR

A

CONTROLS BP. HELPS INCREASE BP VIA VASOCONSTRICTION AND RETAIN BLOOD VOLUME

189
Q

WHAT DOES THE GFR DIRECTLY RELATE TO

A

THE NUMBER OF FUNCTIONING NEPHRONS THAT WE ALSO HAVE IN THE BODY

190
Q

WHAT DOES AN INCREASED CREATININE LEVEL INDICATE

A

LOW GFR SO WE ARE NOT FILTERING AS EFFECTIVELY

191
Q

BUN

A

BLOOD UREA NITROGEN LEVEL

192
Q

NORMAL URINE

A

YELLOW TO AMBER
CLEAR TO SLIGHTLY HAZY
PH 5-6

193
Q

NORMAL URINE PRODUCTION

A

600-2500 ML/D

194
Q

URINE SHOULD BE NEGATIVE FOR

A

GLUCOSE
KETONES
BLOOD
PROTEIN
BACTERIA
WBC
CRYSTALS
RBC
BILIRUBIN

195
Q

WHAT DO WBC IN URINE INDICATE

A

UTI

196
Q

WHAT DOES PROTEIN IN THE URINE INDICATE

A

PROBLEM OR DAMAGE TO OUR GLOMERULUS

197
Q

WHEN DO WE SEE POLYURIA

A

DIURETICS

198
Q

WHEN DO WE SEE OLIGURIA

A

DEHYDRATION
RENAL FAILURE

199
Q

WHEN DO WE SEE ANURIA

A

CHRONIC RENAL FAILURE
COMPLETE OBSTRUCTION

200
Q

WHAT PERCENT OF CARDIAC OUTPUT DO THE KIDNEYS RECEIVE UNDER NORMAL CIRCUMSTANCES

A

20-25 % OR ABOUT 1000-13000 ML/MIN

201
Q

WHAT IS A NORMAL GFR

A

125 ML/MIN
BUT OFTEN JUST LOOKING AT ABOVE 60 OR BELOW 60

202
Q

WHAT FORCES DRIVE GLOMERULAR FILTRATION

A

BP
PROTEIN AND GLUCOSE LEVELS
RAS SYSTEM
SYMPATHETIC NERVOUS SYSTEM
LOSS OF NEPHRONS

203
Q

WHAT HAPPENS TO URINE OUTPUT WITH SYMPATHETIC NERVOUS SYSTEM STIMULATION AND WHY

A

INCREASE IN URINE OUTPUT BECAUSE INCREASE IN HR

204
Q

WHAT LAB TEST IS THE MOST SPECIFIC INDICATOR OF RENAL FUNCTION

A

CREATININE

205
Q

IN RESPONSE TO ACIDOSIS, THE KIDNEYS WILL

A

PRODUCE AND CONSERVE BICARB AND EXCRETE OUR HYDROGEN ACID

206
Q

WHAT IS THE ACTION OF ALDOSTERONE

A

MAKES US RETAIN SODIUM THUS WATER RETENTION

207
Q

WHAT ACTION DO NATRIURETIC PEPTIDES HAVE IN THE KIDNEY

A

PROMOTE RENAL EXCRETION OF SODIUM AND WHERE THAT SALT GOES, WATER WILL FOLLOW

208
Q

IS IT NORMAL TO FIND RBC AND LARGE AMOUNTS OF PROTEIN IN THE URINE

A

NO

209
Q

WHAT SUBSTANCE PRODUCED BY THE KIDNEY WILL PROMOTE RBC PRODUCTION IN THE BONE MARROW

A

ERYTHROPOIETIN

210
Q

WHAT CO FACTOR SYNTHESIZED BY THE KIDNEY IS NEEDED TO PROMOTE THE ABSORPTION OF CALCIUM IN THE GI TRACT

A

VITAMIN D

211
Q

CAUSES OF URINARY OBSTRUCTION

A

PREGNANCY
TUMOR
KIDNEY STONE
SCAR TISSUE
NEUROGENIC BLADDER
BLADDER OUTFLOW OBSTRUCTION
URETEROVESICAL JUNCTION STRUCTURE

212
Q

STAGHORN STONES

A

LARGE STONES THAT FILL THE RENAL PELVIS AND AT LEAST ONE RENAL CALYCES
MOST COMMONLY STRUVITE AND LINKED TO UTI

213
Q

68 y/o, Fx tibia, immobilized for two weeks, Hx of stones. He has excruciating left flank pain. Pt. states pain comes and goes and it intensifies
.– Type of pain – colicky or non-colicky?
– Suggestion as to location of stones?
– Type of stone?

A

A. COLICKY
B. KIDNEY OR UPPER URETER OF LEFT KIDNEY
C. USUALLY CALCIUM PHOSPHATE

214
Q

Who is more at risk for a UTI (female or a male)? Why?

A

FEMALE, SHORTER URETHRA

215
Q

Why are fluids recommended in the treatment of UTI’s?

A

WASHOUT PHENOMENON

216
Q

What factors increase the risk of a UTI in an older adult?

A

MALNUTRITION
DECREASED NEPHRONS
SEDENTARY LIFESTYLE
LOWER ESTROGEN LEVELS

217
Q

Why are UTI’s difficult to diagnose in elderly?

A

UNABLE TO ACCURATELY REPORT
LOWER NORMAL BODY TEMP
PREVALENCE OF ASYMPTOMATIC BACTERIA

218
Q

CLINICAL MANIFESTATIONS OF NEPHRITIC SYNDROME

A

inflammatory response –>hematuria, red cell casts in urine, decreased GFR, azotemia, oliguria, hypertension

219
Q

CLINICAL MANIFESTATIONS OF NEPHROTIC SYNDROME

A

increased permeability ofthe glomerulus – massive protein uria,hypoalbuminemia, generalized edema, lipiduria and hyperlipidemia

220
Q

CLINICAL MANIFESTATIONS OF ASYMPTOMATIC GLOMERULAR DISEASE

A

hematuria, proteinuria aren’t recognized

221
Q

WITH NEPHRITIC SYNDROMES, IS GLOMERULAR INFLAMMATION ACUTE OR CHRONIC

A

ACUTE

222
Q

WHAT HAPPENS WHEN NEPHRITIC SYNDROMES CAUSE OCCLUSION OF THE CAPILLARY LUMEN

A

decrease incapillary permeability, capillary wall damage
– Sudden onset of hematuria, with red blood cell casts

223
Q

WHAT DO WE SEE WHEN NEPHRITIC SYNDROMES CAUSE A DECREASED GFR

A

fluid accumulation, edema, hypertension
* Varying degrees of proteinuria

224
Q
A
225
Q

WHEN GLOMERULAR DAMAGE CAUSES HYPOPROTEINEMIA, WHAT 2 THINGS HAPPEN

NEPHROTIC SYNDROME

A
  1. EDEMA
  2. HYPERLIPIDEMIA
226
Q

HYPOPROTEINEMIA

A

INCREASED PERMEABILITY TO PROTEINS FROM GLOMERULAR DAMAGE

227
Q

PREOTEINURIA LEVELS

A

> 3.5 G/D

228
Q

WHY DOES HYPOPROTEINEMIA CAUSE EDEMA

A

DCREASED PLASMA ONCOTIC PRESSURE

229
Q

WHY DOES HYPOPROTEINEMIA CAUSE HYPERLIPIDEMIA

A

COMPENSATORY SYNTHESIS OF PROTEINS BY THE LIVER

230
Q

Tx OF GLOMERULONEPHRITIS

A
  • Focus on cause
  • Steroids – inflammation, plasmaphresis
  • Dietary, fluid management
  • Treament of HPT
  • If kidney failure – dialysis or transplant
231
Q

PROGRESSION OF Diabetic Glomerulosclerosis

A

Diabetic nephropathy –> glomerulosclerosis –> chronic kidney disease
* Result of the effects of elevated glucose on the glomerulus

232
Q

PATHO OF DIABETIC GLOMERULOSCLEROSIS

A

Widespread thickening of the basement membrane, early increase in GFR –> over time reduces GFR

233
Q

EARLY CHANGE INDICATING DIABETIC GLOMERULOSCLEROSIS

A

MICROALBUMINEMIA

234
Q

Tx of Diabetic Glomerulosclerosis

A

– Control blood glucose levels
– ACE inhibitors or ARBs
– Control of blood pressure
– Smoking cessation

235
Q

Tubulointerstital Diseases

A

Affect renal tubule structures and interstitial tissues surrounding tubules

236
Q
  • Acute tubular necrosis
A

a kidney disorder involving damage to the tubule cells of the kidneys, which can lead to acute kidney failure.

237
Q
  • Acute/chronic pyelonephritis
A

a sudden and severe kidney infection. It causes the kidneys to swell and may permanently damage them. Pyelonephritis can be life-threatening. When repeated or persistent attacks occur, the condition is called chronic pyelonephritis.

238
Q

Pyelonephritis

A

Infection of the renal parenchyma, pelvis
ACUTE OR CHRONIC
CAN ASCEND OR BE HEMATOGENOUS

239
Q

PREDISPOSING FACTORS OF PYELONEPHRITIS

A

vesicoureteral reflux, pregnancy, neurogenic bladder, catheterization instrumentation

240
Q

Pyleonephritis – Clinical Manifestations

ACUTE

A

Chills, fever
* Headache
* Flank,back pain
* Dysuria, frequency urgency
* Malaise
* Costovertebral angle tenderness

241
Q

Pyleonephritis – Clinical Manifestations

CHRONIC

A
  • History of recurrent UTI
  • Can be same as for acute or
  • Polyuria
  • Nocturia
  • Mild proteinuria
  • Hypertension
242
Q

Wilms tumor (nephroblastoma)

RENAL CARCINOMA

A

– Children 3-5 years.
– Associated with chromosomal abnormality (5%)
– Abdominal mass, hypertension, abd. pain, vomiting
– Diagnosis: ultrasound, CT
– Treatment – surgery, chemo, radiation

243
Q

RENAL CELL CARCINOMA

A

– Adults 60-70’s
– Hematuria, flank pain, palpable flank mass
– Diagnosis: ultrasound, CT
– Treatment: surgical resection

244
Q

Acute Kidney Injury

A

Sudden severe decrease inrenal function that ispotentially reversible

245
Q

PRERENAL

ACUTE KIDNEY INJURY TYPES

A

decreased blood flow to kidney

246
Q

Intrarenal (intrinsic)

ACUTE KIDNEY INJURY TYPES

A
  • damage to the structures within the kidney (nephrons)
247
Q

Postrenal

ACUTE KIDNEY INJURY TYPES

A

– interference with urine outflow

248
Q

WHAT CAUSES INTRINSIC ACUTE KIDNEY INJURY

A

DAMAGE TO THE STRUCTURES WITHIN THE KIDNEY

249
Q

WHAT CAUSES PRERENAL ACUTE KIDNEY INJURY

A

MARKED DECREASE IN RENAL BLOOD FLOW

250
Q

WHAT CAUSES POSTRENAL ACUTE KIDNEY INJURY

A

OBSTRUCTION OF URINE OUTFLOW FROM THE KIDNEY

251
Q

Decreased renal perfusion

PRERENAL AKI

A

– Hypovolemia – hemorrhage, dehydration
– Decreased cardiac output – heart failure, anaphylactic or septic shock

252
Q

CAN PRERENAL AKI BE REVERSED

A

YES, IF CAUSE IS QUICKLY IDENTIFIED AND TREATED

253
Q

NEPHRONS

PRERENAL AKI

A

functional, but decreased blood flow results in decreased GFR. (results with prolonged mean arterial pressure <70 mm Hg.)

254
Q

What is an indicator of tissue perfusion that might provide a cue about a pre-renal problem?

A

PROTEIN IN THE URINE INDICATED NEPHRON DAMAGE

255
Q

Intrarenal (Intrinsic)

AKI

A
  • Damage to the renal parenchyma (nephron -glomerulus or tubules injured)
  • Longer course of recovery, or progression to chronic renal failure
256
Q

CAUSES OF INTRARENAL (INTRINSIC) AKI

A

– Prolonged ischemia
– Exposure to nephrotoxic agents
– Intratubular obstruction (myoglobinuria, myeloma)
– Inflammatory process – glomerulonephritis, pyelonephritis

257
Q

Acute Tubular Injury or Necrosis Intrarenal

A

Destruction of the tubular epithelial cells leading to acute impairment of renal function

258
Q

Acute Tubular Injury or Necrosis Intrarenal

CAUSES

A

extensive surgery, severe hypovolemia, sepsis, trauma, burns, intratubular obstructions – myoglobin or hemoglobinuria

259
Q

ATN - Patho

A

Ischemic/toxic insult->
tubular epithelial cellinjury ->
release “debris” intotubular lumen-> lumen obstructed -> tubular pressure increases -> pressure in Bowman’s capsule increases -> glomerular filtration slowed ->Pressure not relieved ->“back leak” into the interstitium -> decreased perfusion -> kidneys become hypoxic

260
Q

Postrenal AKI

A

Outflow obstruction within the urinary collecting system distal to the kidneys (ureters, bladder, urethra)

261
Q

Postrenal AKI CAUSES

A

BPH, stones, UTI, tumors, strictures, altered bladder contraction

262
Q

POSTRENAL AKI PROGRESSION

A

Obstruction -> increased interstitial pressure -> elevated Bowman’s capsule pressure-> impedes filtration -> GFR decreased

263
Q

POSTRENAL AKI TREATMENT

A

REMOVAL OF OBSTRUCTION

264
Q

Onset

AKI PHASES

A

– precipitation event until tubular injury

265
Q
  • Oliguric (anuric)

AKI PHASES

A

– GFR falls, nitrogenous wastes accumulate (azotemia), hyperkalemia urine output decreases (oliguria, anuria) -> fluid retention

266
Q
  • Diuretic

AKI PHASES

A

– GFR increases, healing, urine output increases

267
Q
  • Recovery

AKI PHASES

A

– tubular edema resolves, GFR improves (70-80% of normal), urine output and blood levels of nitrogenous wastes return to normal
* Note – some damage may persist

268
Q

Hallmarks of Acute Kidney Injury

A
  • Decreased glomerular filtration rate
  • Azotemia
  • Decreased urine output (oliguria, anuria)
269
Q

RISK FACTORS OF AKI

A

Pre-existing renal impairment, atherosclerosis, hypertension, diabetes, HF, age

270
Q

MORTALITY OF AKI

A

15-60%

271
Q

AKI NURSING CONSIDERATIONS

A

Prevention
* Early diagnosis – identify the cause, watch for symptoms
* Monitor urine output
* Urine tests – UA, specific gravity, osmo
* Blood tests – BUN, Cr, electrolytes
* Adequate nutrition and rest

272
Q

HOW DO YOU PROTECT THE KIDNEY IN AKI

A

– Prevention of infections
– Monitor use of nephrotoxic drugs (ie: aminoglycosides, radiocontrast agents etc.)
* Dialysis or continuous renal replacement therapy (CRRT)

273
Q

Does Kidney failure equal end stage renal disease

A

no

274
Q

what is chronic renal failure

A

Progressive loss of renal function over months to years due to permanent loss of nephrons

275
Q

is chronic renal failure reversible

A

not as reversible as aki

276
Q

can chronic renal failure be slowed

A

yes

277
Q

when does chronic renal failure become irreversible

A

end stage renal disease

278
Q

two main causes of chronic renal failure

A

diabetes and hypertension

279
Q

mortality rate of chronic renal failure

A

100% without dialysis or transplant

280
Q

stages of chronic kidney disease correspond to

A

degree of nephron loss

281
Q

stage 1 of chronic kidney disease

A

kidney damage with normal or increased gfr >90 ml/min

282
Q

stage 2 chronic kidney disease

A

decreased gfr
kidney damage with mild decrease in gfr
60-89 ml/min

283
Q

stage 3 of chronic kidney disease

A

gfr <60 ml/min for 3 months or longer
moderate decrease in gfr- 30-59 ml/min

284
Q

stage 4 chronic kidney disease

A

gfr <60 ml/min for 3 months or longer
severe decrease in gfr 15-29 ml/min

285
Q

stage 5 of chronic kidney disease

A

kidney failure
<15 ml/min

286
Q

nervous system

systemic effects of uremia

A

changes in alertness, level of consciousness, neuropathy –>muscle weakness, restless leg syndrome

287
Q

cardiovascular

systemic effects of uremia

A

decreased cardiac output, pericarditis, hpt

288
Q

hematologic

systemic effects of uremia

A

anemia, bleeding tendencies

289
Q

immune

systemic effects of uremia

A

infection

290
Q

gi

systemic effects of uremia

A

anorexia, n&v

291
Q

skin

systemic effects of uremia

A

pruritus, uremic frost

292
Q

other

systemic effects of uremia

A

sexual dysfunction

293
Q

why are chronic renal failure patients at risk for hypertension

A

Diseased kidneys are less able to help regulate blood pressure. As a result, blood pressure increases.

294
Q

why are chronic renal failure patients at risk for hyperkalemia

A

Reductions in urinary potassium excretion that occur in CKD can lead to an inability to maintain potassium homeostasis.

295
Q

why are chronic renal failure patients at risk for anemia

A

their kidneys cannot make enough erythropoietin which causes their red blood cells to drop and anemia. Most such patients develop anemia, which can happen early in the illness and worsen with time.

296
Q

why are chronic renal failure patients at risk for acidosis

A

the kidneys can’t remove enough acid, which can lead to metabolic acidosis. The normal level of serum bicarbonate is 22-29 mEq/L. Kidney experts recommend that patients not have their serum bicarbonate levels fall below 22 mEq/L

297
Q

why are chronic renal failure patients at risk for uremia

A

uremic solutes accumulate in the circulation owing to deficient renal clearance. Some of these products are considered uremic toxins and are believed to contribute to the uremic syndrome.

298
Q

why are chronic renal failure patients at risk for hyperparathyroidism

A

Defect in the activation of vitamin D in the kidneys due to chronic kidney disease (CKD) leads to hypocalcemia and hyperphosphatemia, resulting in a compensatory increase in parathyroid gland cellularity and parathyroid hormone production and causing secondary hyperparathyroidism (SHP)

299
Q

What happens to H ions in renal failure? how does this affect ph

A

H+ retention in CKD decreases the pH of the kidney interstitial and intracellular compartments,

300
Q

Why do patients with uremia experience neuropathy and severe muscle weakness?

A

Kidney disease and dialysis can lead to neuropathy pain and muscle atrophy. The exact reasons for this are unknown but several possible causes exist. They include vitamin and mineral imbalances, added pressure from dialysis, and overlapping conditions.

301
Q

treatment of chronic kidney disease

A

slow progression
transplantation
dialysis

302
Q

types of dialysis

A

hemodialysis
peritoneal
continuous renal replacement therapy

303
Q

hemodialysis

A

a machine filters wastes, salts and fluid from your blood when your kidneys are no longer healthy enough to do this work adequately.

304
Q

peritoneal dialysis

A

During peritoneal dialysis, a cleansing fluid called dialysate passes through a catheter tube into part of the abdomen known as the peritoneal cavity. The dialysate absorbs waste products from blood vessels in the lining of the abdomen, called the peritoneum. Then the fluid is drawn back out of the body and discarded.

305
Q

crrt dialysis

A

CRRT is a slower type of dialysis that puts less stress on the heart. Instead of doing it over four hours, CRRT is done 24 hours a day

306
Q

kidney transplant

A
  • Patients with ESRD
  • Availability of organs
  • Two types of donors– Living related– Cadaver
  • Renal transplant success superior to any other organ transplant
307
Q

FUNCTIONS OF THE GI SYSTEM

A
  1. PROVIDE NUTRIENTS FOR THE BODY THROUGH
    A. GI MOTILITY
    B. SECRETION OF DIGESTIVE JUICES, ENZYMES, AND HORMONES
    C. DIGESTION OF NUTRIENTS
    D. ABSORPTION OF NUTRIENTS
308
Q

GI MOTILITY

A

PROPULSIVE AND MIXING MOVEMENTS

309
Q

MUCOSA

LAYERS OF THE GI TRACT

A
  1. EPITHELLIUM
  2. LAMINA PROPRIA
  3. MUSCULAR MUCOSAE
    *INNERMOST LAYER
    *ABSORPTIVE FUNCTION OCCURS HERE
310
Q

SUBMUCOSA

GI TRACT LAYERS

A

RIGHT BELOW THE MUCOSA

311
Q

THIRD LAYER OF THE GI TRACT

A

MUSCULARIS PROPRIA- INNER CIRCULAR MUSCLE LAYER, INTERMUSCULAR SPACE, AND OUTER LONGITUDINAL MUSCLE LAYER

312
Q

4TH LAYER OF THE GI TRACT

A

SEROSA

312
Q

WHAT DOES THE MUSCULARIS EXTERNA INCLUDE

A

LONGITUDINAL MUSCLE
CIRCULAR MUSCLE

313
Q

WHAT IS THE SEROSA MADE OF

A

CONNECTIVE TISSUE

314
Q

MESOTHELIUM OF THE GI TRACT

A

SEROSA

315
Q

WHAT DOES GI MOTILITY DO

A

PROPELS FOODS AND FLUIDS THROUGH THE SYSTEM
INTESTINAL SMOOTH MUSCLE- INTRINSIC PACEMAKER- SLOW WAVE ACTIVITY

316
Q

WHAT REGULATES GI MOTILITY

A

ANS AND LOCAL (ENTERIC) SYSTEMS

317
Q

WHAT ENTERIC SYSTEM REGULATES THE GI SYSTEM

A

AUERBACH’S PLEXUS
MEISSNER’S PLEXUS

318
Q

AUERBACH’S PLEXUS

A

CONTROLS MOTILITY

319
Q

MEISSNER’S PLEXUS

A

CONTROLS SECRETION AND BLOOD FLOW

320
Q

PARASYMPATHETIC SYSTEM AND THE GI SYSTEM

A

VAGUS NERVE –> INCREASE MOTILITY –> SECRETORY ACTIVITIES

321
Q

SYMPATHETIC NERVOUS SYSTEM AND THE GI SYSTEM

A

aravertebral, celiac, superior and inferior mesenteric ganglia –> sphincter control, decrease motility and secretory activities

322
Q

Cholecystokinin

A

stimulates contraction of gallbladder, secretion of pancreatic enzymes, slows gastric emptying

323
Q

SECRETIN

A

Stimulates secretion of bicarb solution from pancreas and liver

324
Q

Glucagon-like peptide I (GLP-1)

Incretin hormones

A

augments insulin release, suppresses glucagon release, slows gastric emptying, decreases appetite

325
Q

Glucose dependent insulinotropic polypeptide (GIP) – augments insulinrelease

Incretin hormones

A

– augments insulin release

326
Q

GASTRIN

A

Stimulates gastric acid, pepsinogen secretion, increases gastric blood flow, stimulates smooth muscle contraction and growth of mucosa

327
Q

GHRELIN

A

STIMULATES SECRETION OF GROWTH HORMONE, STIMULATES APPETITE

328
Q

WHAT DOE EPITHELIAL CELLS SECRETE

A

MUCOUS FOR PROTECTION

329
Q

WHAT DO PARIETAL (OXYNTIC) CELLS SECRETE

A

HCL AND INTRINSIC FACTOR

330
Q

WHAT DO CHIEF (PEPTIC) CELLS SECRETE

A

PEPSINOGEN

331
Q

WHAT DO G CELLS SECRETE

A

GASTRIN

332
Q

Prostaglandins - Serve a protective function in the stomach and duodenum by:

A
  1. STIMULATING THE SECRETION OF MUCOUS AND BICARB
  2. SUPRESSING THE SECRETION OF GASTRIC ACID
  3. PROMOTING SUBMUCOUSAL BLOOD FLOW BY VASODILATION (PROMOTES EPITHELIAL CELL REGENERATION
333
Q

WHAT SUBSTANCES CAN BE DAMAGING TO THE MUCOUSAL BARRIER

A

NASAIDS, HELIOBACTER PYLORI, ALCOHOL, BILE SALTS
THEY ALLOW THE HYDROGEN ION ENTRY INTO THE TISSUE THAT RESULTS IN TISSUE DAMAGE

334
Q

IS THE GUT STERILE

A

NO

335
Q

WHY DOES THE STOMACH AND SMALL INTESTINE ONLY CONTAIN A FEW SPECIES OF MICROORGANISMS

A

VERY ACIDIC. MANY DON’T SURVIVE ALL THE WAY TO THE SMALL INTESTINE

336
Q

WHERE IS THE LARGEST ECOSYSTEM OF MICROBES IN THE GI TRACT FOUND

A

COLON: PART OF THE LARGE INTESTINE. PRIMARILY ANAROBIC. 300-500 SPECIES

337
Q

WHAT ROLE DO THE MICROORGANISMS PLAY IN THE GI TRACT

A

HELP FERMENT DIETARY RESIDUE, HELPS PREVENT EXOGENOUS INFECTION

338
Q

WHAT MIGHT CAUSE A DISRUPTION OF INTESTINAL FLORA AND LEAD TO OPPORTUNISTIC INFECTION

A

ANTIOBIOTICS- SPECIFICALLY BROAD SPECTRUM

339
Q

GI IMMUNITY

A

DAILY CONTACT WITH EXTERNAL ENVIRONMENT
PATHOGENS AND TOXIC SUBSTANCES
GI IMMUNE STRUCTURES HELP TO PREVENT SUBSTANCES FROM ENTERING BLOOD/LYMPH

340
Q

FACTORS OF GI IMMUNITY

A

LOW PH IN THE STOMACH
IMMUNOGLOBULINS IN MUCOUS
GALT
MICROFOLD CELLS

341
Q

GALT
GUT ASSOCIATED LYMPHOID TISSUES

A

PEYER’S PATCHES
LYMPHOCYTES THROUGHOUT GUT

342
Q

Name the three sections of the small intestine

A
  1. DUODENUM
  2. JEJUNUM
  3. ILEUM
343
Q

What happens when you don’t have intrinsic factor?

A

ISSUES ABSORBING VITAMINS LIKE B12 LEADING TO ANEMIAS

344
Q

What is the action of pepsin?

A

AID IN DIGESTION
SPECIFICALLY BREAKING DOWN PROTEINS

345
Q

What is the name of the sphincter located between the stomach and the small intestine?

A

PYLORIC SPHINCTER

346
Q

What type of acid-base problem would you anticipate having if you have had frequent prolonged vomiting?

A

METABOLIC ALKALOSIS

347
Q

What layer of the GI tract contains blood vessels, nerves and structures responsible for secretion of digestive enzymes

A

SUBMUCOSAL

348
Q

What is the form that protein needs to be in order to be used by the body?

A

AMINO ACIDS
THIS IS WHAT PEPSIN BREAKS IT INTO

349
Q

What are the four parts of the colon?

A
  1. SIGMOID
  2. ASCENDING
  3. TRANSVERSE
  4. DESCENDING
350
Q

What structure covers the larynx and prevents aspiration when swallowing?

A

EPIGLOTTIS

351
Q

In what part of the GI tract does the majority of nutrient absorption occur?

A

SMALL INTESTINE

352
Q

Liver

A
  • Secretion of bile - HEPATOCYTES
  • GETS LIKE 20% OF CARDIAC OUTPUT
  • Metabolism of bilirubin
  • Vascular/hematologic function
  • Metabolism of nutrients
  • Metabolic detoxification
  • Storage of mineral and vitamins
353
Q

Gallbladder

A

 Stores and concentrates bile between meals
 Bile from liver via hepatic ducts

354
Q

 Pancreas

A

 Secretes enzymes and alkaline fluids that digest proteins, carbs, and fats

355
Q

Choleresis

A

=bile secretion

356
Q

WHAT DOES BILE CONTAIN

A

bile salts required for intestinal emulsification and absorption of fats

357
Q

FAT SOLUABLE VITAMINS

A

D, E, K, A

358
Q

HOW MUCH BILE DOES THE LIVER SECRETE A DAY

A

700-1200 ML/DAY

359
Q

WHAT IS BILIRUBIN A BYPRODUCT OF

A

DESTRUCTION OF OLD RB’S
Gives bile its color and produces yellow tinge of jaundice

360
Q

HOW IS BILIRUBIN EXRETED

A

MOSTLY IN URINE

361
Q

KUPFFER CELLS

A

MACROPHAGES THAT TAKE UP AND DESTROY AGED RBCs AND CONVERT THEM TO BILIRUBIN

362
Q

Vascular/Hematologic Functions

LIVER

A

 Stores large volumes of blood
 Kupffer cells important in destroying intestinal bacteria and preventing infection
 Synthesizes prothrombin, fibrinogen, and factors I, II,VII, IX, and X
 Vit K depends on adequate bile production

363
Q

Anorexia

A

– loss of appetite, lack of desire to eat, despite the normal physiologic stimuli

364
Q

 Factors influencing appetite:

A

hunger, smell, emotions, drugs, disease states

365
Q

 Nausea

A

– unpleasant, subjective, conscious sensation resulting from stimulus of the medullary vomiting center

366
Q

 Common cause of nausea:

A

distention of duodenum

367
Q

 nausea is Accompanied by autonomic nervous system responses:

A

watery saliva, pallor, sweating, elevated heart rate

368
Q

regulation of vomiting

A

in medulla
 Chemoreceptor trigger zone, Vomiting center

369
Q

stimuli that can result in vomiting

A

Distention or irritation of the stomach, small intestine
 Stimulation of the vestibular system in the inner ear (motion sickness, ear infection etc.)
 Blood-borne emetics/toxins (chemotherapy, opioids, ipecac)
 Sensory input (sight, smell, pain)
 Hypoxia (decreased CO, shock, increased intracranial pressure)

370
Q

vomiting patho

A

Airway closed, forceful contraction of diaphragm/abd. muscle, gastroesophageal sphincters relax

371
Q

dysphagia

A

Difficulty swallowing
May include inability to initiate swallowing or sensation that swallowed foods “stick

372
Q

causes of dysphagia

A

Problem in food delivery into esophagus (neuromuscular incoordination)
Problem with transport down the esophagus (altered peristaltic activity)
Problem with entry into stomach (LES dysfunction or obstructing lesions)

373
Q

DIARRHEA

A

Increase in the frequency and fluidity of bowel movements. Symptom of GI disease

374
Q

types of acute diarrhea

A

inflammatory
noninflammatory

375
Q

causes of diarrhea

A

nfection, maldigestion, inflammation, functional disorders

376
Q

complications of diarrhea

A

dehydration
electrolyte imbalances

377
Q

management of diarrhea

A

 Diagnosis and treatment of the underlying cause
 Replacement of lost water and electrolytes
 Relief of cramping
 Reducing the passage of unformed stools

378
Q

CONSTIPATION

A

Small, infrequent, incomplete or difficult passage of stool

379
Q

Impaction:

A

firm, immovable mass of stool that becomes stationary in the GI

380
Q

Constipation causes

A

 Low residue (fiber) diet
 Lack of exercise (sedentary lifestyle, bedrest)
 Slowed peristalsis (elderly, excessive use of opioids)
 Conditions that alter GI motility (spinal cord injuries, MS, endocrine)
- Medications (opioids, anticholinergics

381
Q

GASTROESOPHAGEAL REFLUX

A

Symptoms or mucosal damage caused by abnormal reflux of gastric contents into esophagus
Weakening of lower esophageal sphincter

382
Q

Persistent reflux =

A

esophagitis, reflux disease

383
Q

gerd

A

 Weak, incompetent LES
 Irritation effects of refluxate (ph <4.0)
 Decreased clearance of refluxate from the esophagus
 Mucousal injury, hyperemia, inflammation
 Progressive disease -> erosive esophagitis Barrett’s esophagus

384
Q

barrett’s esophagus

A

– metaplasia squamous mucosa, replaced by abnormal columnar epithelial cells
 increased cancer risk

385
Q

gerd Clinical manifestations:

A

 heartburn
 regurgitation
 belching
 pain
 bleeding
 respiratory symptoms

386
Q

gerd Tx

A

 Weight reduction
 Avoid large meals
 Decrease in foods/activities that decrease LES tone (caffeine, fats, chocolate, ETOH, smoking)
 Avoid activities that increase IAP (lifting)
 Positioning (elevate HOB, upright after eating)
 Medications
 Surgical intervention

387
Q

does everyone who has gastroesophagealreflux have GERD?

A

no

388
Q

Is there an association between GERD and asthma?

A

yes

389
Q

why would sitting up help to relieve the symptoms of gerd

A

gravity, keeps it down

390
Q

what are the complications of gerd

A

burning of esophagus
pain

391
Q

BALANCING THE SCALE- GASTRIC MUCOSAL BARRIER

agressive factors

A

age
smoking
alcohol
bile acids from duodenal reflux
h pylori
nsaids
acid
pepsin

392
Q

gastric mucosal barrier

defensive factors

A

mucus
bicarb
blood flow
prostaglandins

393
Q

esophagitis

A

inflammation of esophagus from gerd

394
Q

pyloris

A

heartburn

395
Q

Hematemesis

A

– bloody vomitus (bright red or coffee ground)

396
Q

Melena

A

– blood in the stool (bright red to tarry black)

397
Q

Occult blood

A

– blood in the stool that is not apparently visible

398
Q

Hematochesia

A

– fresh blood from the stool

399
Q

causes of acute gastritis

A

ingestion of alcohol, aspirin/NSAIDS, viral, bacterial or chemical toxins, glucocorticoids, profound stress

400
Q

causes of chronic gastritis

A

helicobacter pylori, atrophic (autoimmune, environmental), chemical gastropathy (alkaline reflux)

401
Q

clinical manifestations of gastritis

A

Anorexia, nausea, vomiting, occ. Blood, Hematemesis, abd. pain

402
Q

Tx of acute gastritis

A

remove causative agent

403
Q

Tx of chronic gastritis

A

reat H. pylori (antimicrobials)

404
Q

PEPTIC ULCER DISEASE

A

Disorders of the GI tract (stomach, duodenum) caused by action of acid and pepsin
Range -> slight injury -> severe ulceration
Can affect one or multiple layers
Imbalance of defensive (protective) factors vs. aggressive factors

405
Q

Two major causes of gastric irritation and ulceration

A

– H. pylori, aspirin, other NSAIDS

406
Q

peptic ulcer disease- clinical manifestations

A

 Epigastric burning, discomfort, pain
 Nausea
 Abdominal upset

407
Q

peptic ulcer disease-diagnosis

A

H&P, endoscopy, H.pylori test labs, radiographic studies

408
Q

Tx of peptic ulcer disease

A

 Pharmacologic – eradicate cause, relieve ulcer symptoms, heal the ulcer
 Prevent complications
 Avoidance of injurious agents
 Diet: avoid foods that cause symptoms

409
Q

complications of peptic ulcer disease

A

hemorrhage, gastric outlet obstruction, perforation

410
Q

INFLAMMATORY BOWEL DISEASE

2 diseases

A

crohns disease
ulcerative colitis

411
Q

inflammatory bowel disease

chronic illness

A

remissions and exacerbations

412
Q

onset of ibd

A

childhood to young adulthood

413
Q

causes of ibd

A

autoimmune, genetic predisposition, environmental trigger - microbial flora

414
Q

how is ibd diagnosed

A

colonoscopy

415
Q

ulcerative colitis

ibd

A

Ulcerative, exudative
Primarily mucousal
Continuous lesions
Rectum, left colon
Diarrhea - common
Rectal bleeding -common
Fistulas, strictures, abscesses -rare
Increased risk of colon cancer

416
Q

chron’s disease

A

Granulomatous
Primarily submucousal
Skips lesions - cobblestone
Primary ileum, then colon
Diarrhea – common;
Rectal bleeding - rare
Strictures, fistulas, abscesses -common
Cancer risk- uncommon

417
Q

ibd diagnosis

A

History/physical, colon/sigmoidoscopy, biopsy, stool exams

418
Q

Tx of ibd

A

 Reduction of inflammation (control not cure)
 medications
 Maintaining adequate nutrition
 Preventing complications
 Surgical intervention
 Removal of diseased portion of bowel

419
Q

diverticular disease

A

Outpouchings through the muscular layer of the colon wall
 Often found in descending/sigmoid colon

420
Q

diverticular disease

patho

A

high intraluminal pressure on areas of bowel wall weakness

421
Q

diverticular disease

causes

A

ow fiber diet, lack of exercise, poor bowel habits, aging

422
Q

diverticular disease

progression

A

Inflamed diverticula -> diverticulitis -> fever, lower abd. pain ->abscess development, peritonitis, obstruction

423
Q

diverticular disease

Tx

A

diet,“itis” -> antibiotic, fluids, electrolytes, surgery –unresolved symptoms, complications

424
Q

intestinal obstruction

A

Partial or complete blockage of the small or large intestinal lumen –impaired movement

425
Q

types of intestinal obstruction

A

mechanical
paralytic

426
Q

intestinal obstruction

clinical manifestations

A
  • Mechanical: increased bowel sounds, abd. pain, colicky, nausea
  • Paralytic: absence of bowel sounds
  • Both: pain, constipation, abd. distention, vomiting
427
Q

intestinal obstruction

diagnosis

A

h and p
abd xray
ct
us

428
Q

intestinal obstruction

complications

A

edema
ischemia
necrosis
perforation

429
Q

intestinal obstruction

Tx

A

decompression or surgical intervention, correction of fluid and electrolyte imbalances

430
Q

PERITONITIS

A

Inflammatory response of the serous membrane

431
Q

peritonitis

causes

A

chemical irritation
bacteria

432
Q

peritonitis

symptoms

A

pain, tenderness, rigid/boardlike abdomen, vomiting, fever, tachycardia, hypotension, elevated WBC, hiccups, paralytic ileus

433
Q

peritonitis

rx

A

correct cause, antibiotics, decompression, fluid and electrolyte replacement, nothing by mouth, pain control

434
Q

COLORECTAL CANCER

A

 2nd leading cause of cancer deaths in US
 Seen in those in 40’s, mean age 68 men, 72 women
 Adenomatous polyps thought to be a precursor

435
Q

polyp

A

benign neoplasm, from mucosal epithelium of the intestine

436
Q

cause of colorextal cancer

A

unknown, incidence
 increases with age, familial risk, diet, ulcerative colitis

437
Q

screening for colorectal cancer

A

 40 – digital rectal exam annually
 50 – fecal occult blood test annually, sigmoidoscopy every five years , barium enema every five years or colonoscopy every 10.
 High risk – screen earlier
 Colonoscopy with positive screen

438
Q

hepatitis

A

Inflammation/infection of the liver by hepatotoxic viruses

439
Q

types of hepatitis

A

 A (spread by fecal-oral route)
 B (spread by blood, body secretions/oral/sexual contact)
 C (spread by blood)

440
Q

clinical minifestations of hepatitis

A

N/V/D, elevated liver enzymes, elevated bilirubin, liver tenderness

441
Q

Tx of hepatitis

A

antivirals, minimize risk factors, prevention via immunizations

442
Q

LIVER—CIRRHOSIS

A

End stage liver disease with loss of functional liver tissue

443
Q

LIVER—CIRRHOSIS

causes

A

Causes: etoh, hepatitis, toxicity from drugs/chemicals

444
Q

LIVER—CIRRHOSIS

clinical manifestations

A

vary, asymptomatic to end stage liver failure
 Weight loss, anorexia, weakness, diarrhea, hepatomegaly, jaundice, portal hypertension

445
Q

portal hypertension

A

increased resistance to flow in the portal venous system

446
Q

LIVER—CIRRHOSIS

complications

A

include ascites, splenomegaly, hepatic encephalopathy ,and esophageal varices

447
Q

Cholecystitis

gallbladder

A

 acute or chronic inflammation of the gallbladder (commonly due to obstruction of gallbladder outlet

448
Q

acute Cholecystitis s/s

gallbladder

A

RUQ/epigastric pain, mild fever, anorexia, nausea, vomiting, elevated WBC, elevated liver enzymes, elevated bilirubin

449
Q

chronic Cholecystitis s/s

gallbladder

A

more vague—intolerance of fatty foods, belching, GI discomfort, possible enlargement of gallbladder

450
Q

diagnosis of gallbladder

A

US, CT scans; treated by surgical cholecystectomy if needed

451
Q

Cholelithiasis

A

gallstones
Generally caused by buildup of cholesterol or bilirubin

452
Q

Cholelithiasis

contributing factors

A
  • Contributing factors: abnormal bile composition and bile stasis
453
Q

Cholelithiasis

s/s

A

many are asymptomatic until stones are large, may see obstruction, jaundice, biliary colic

454
Q
A

312 Patho (3 decks)

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