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Bioscience 2 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Name the 4 walls of the GI tract from innermost to outermost

A
  1. Mucosal layer
  2. Submucosal Layer
  3. Muscularis layer
  4. Serosal layer
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2
Q

What are the 3 subcomponents of the mucosal layer of the GI tract

A
  • epithelium
  • lamina propria (CT that contains capillaries and lacteals)
  • muscularis mucosae (not important for motility, increases SA)
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3
Q

Describe the Submucosal layer

A
  • connective tissue
  • blood vessels, secretory glands and neurons
  • submucosal plexus of Meissner’s plexus (post-ganglionic parasympathetic neurons)
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4
Q

Muscular layer

A

-inner muscle layer is circular and wraps tube
contractions narrow the tube
-outer layer contractions shorten and increase diameter of tube

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5
Q

Where is the myenteric plexus / Auerbachs plexus found

A
  • muscluaris layer

- post ganglionic parasympathetic neurons

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6
Q

Parasymp and Symp in GI

A
  • parasymp is stimulatory

- symp is inhibitory

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7
Q

What are the functions of saliva

A
  • chemical digestion of CHO and some lipids
  • lubrication of GI tract, aids in bolus formation
  • enhances taste
  • keeps mouth and teeth clean
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8
Q

How is saliva production stimulated

A

-parasymp, produces copious watery saliva
-smell
sour foods
local reflexes

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9
Q

Sjogren’s syndrome

A
  • lymphocyte and plasma cells invade salivary and lacrimal glands
  • dry mouth and eyes
  • rheumatoid arthritis, lupus, scleroderma
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10
Q

What does the esophagus do?

A

moves bolus of food from mouth to stomach via peristalsis

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11
Q

Describe the cells in the esophagus

A
  • proximal 1/3 is skeletal muscle, remainder is smooth muscle
  • stratified squamous epithelium
  • secretes mucus
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12
Q

Gastroesophageal Junction

A

abrupt transition from stratified epithelium to pseudo columnar epithelium (in stomach)
-lower esophageal sphincter is here

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13
Q

Lower Esophageal Sphincter

A
  • anatomically distinct form surrounding smooth muscle

- allows ingested food into stomach and prevents stomach contents into esophagus

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14
Q

Gastroesophageal Reflux Disease (GERD)

A
  • heartburn that occurs twice per week
  • pain in upper/mid abdomen can radiate to chest, throat, shoulder, back
  • made worse after eating large meals
  • worse at night
  • respiratory symptoms
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15
Q

GERD treatment

A
  • stop smoking
  • stop drinkin
  • lose weight
  • wear looser clothing
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16
Q

Barretts esophagus

A
  • conversion of esophageal mucosa to intestinal mucosa after repeated exposure to gastric contents
  • occurs in 10-15% ppl w/ GERD
  • risk factor for esophageal cancer (adenocarcinoma)
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17
Q

Esophageal Cancer (adenocarcinoma)

A
  • dysphagia and weight loss
  • white males
  • distal 1/3 of esophagus
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18
Q

Esophageal Cancer (squamous cell carcinoma)

A

-alcohol and smoking
-blacks
better prognosis

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19
Q

What makes pepsinogen

A

-chief or zymogenic cells

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20
Q

What do parietal cells do in the stomach

A
  • make HCl

- make intrinsic factor

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21
Q

What does intrinsic factor do

A

-necessary for vitamin B12 absorption

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22
Q

Pernicious anemia

A

-lack of vitamin B12 from diet or intrinsic factor

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23
Q

Basic electrical rhythm of stomach

A
  • generates peristaltic contractions
  • pacemaker cells in longitudinal muscle layer generate contractions
  • 3-5 contractions/minute
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24
Q

What is the role of the pyloric sphincter

A
  • regulates outflow from stomach into duodenum

- only a small amount with each contraction 2-3mLs

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25
Q

Pepsinogen

A
  • secreted by chief cells in the gastric pits
  • active form is pepsin
  • protease
  • pepsin also activates more pepsin from pepsinogen
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26
Q

Hydrochloric acid HCl

A
  • produced by parietal cells
  • kills consumed microbes
  • pH ranges 0-4 average 2
  • low pH denatures proteins
  • activates pepsin from pepsinogen
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27
Q

What simulates pepsinogen and HCl secretion?

A
  • parasympathetic stimulation
  • stomach distention
  • protein
  • histamine
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28
Q

What inhibits pepsinogen and HCl

A

increased duodenal activity

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29
Q

Acute gastritis

A

local irritation from alcohol, NSAIDs, bacterial endotoxins

  • can include erosion of mucosa
  • self limiting
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30
Q

Chronic gastritis

A
  • no visible lesions
  • chronic inflammatory changes that lead to atrophy of glandular epithelium
  • increased risk for stomach cancer
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31
Q

Peptic Ulcer disease

A

-disruption of the mucosal barrier and exposure of underlying tissue to HCl and pepsin can result in ulceration of epithelium

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32
Q

Where does peptic ulcer disease occur?

A

-duodenal ulcers are 5X more common that gastric ulcers

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33
Q

Symptoms of peptic ulcer disease

A

-pain worse when empty stomach
-bleeding can occur
-

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34
Q

What is the goal of GERD and peptic ulcer Pharm

A

-reduce acid secretion, protect mucosa, prevent further damage and allow healing

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35
Q

H2 receptor blockers

A
  • inhibits binding of histamine to H2 receptors
  • suppresses HCl secretion
  • decreases gastric acid secretion
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36
Q

H2 receptor side effects

A

-fatigue
-muscle pain
-GI upset,
CNS symptoms in older adults
-many drug interactions

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37
Q

Proton pump inhibitors

A
  • prodrug, converted to active form in stomach
  • binds to H+/K+ ATPase of parietal cells
  • more effective/expensive than H2 blockers
  • increased fracture risk
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38
Q

Carafate

A
  • coating agent that bonds to protons, adheres to luminal surface of stomach
  • not absorbed and doesn’t change pH
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39
Q

Pepto-bismol

A
  • barrier forming

- stimulates bicarbonate and PGE2 secretion which inhibits H pylori growth

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40
Q

Cytotec

A
  • coating agent
  • abortion in pregnant
  • not better
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41
Q

Symptoms of stomach cancer

A
  • indigestion
  • weight loss
  • vomiting
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42
Q

Duodenum

A
  • most important segment for digestion and absorption
  • large SA
  • produces bicarbonate that neutralizes gastric enzymes released into duodenum
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43
Q

Brush border Enzymes

A

membrane bound enzymes on the surface of absorptive cells in the small intestine

  • perform final breakdown of consumed nutrients
  • break down disaccharides into monosacs
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44
Q

Brunners gland

A
  • produces alkaline mucus
  • sensitive to sympathetic stimulation
  • inhibits production of alkaline mucus
  • can cause inappropriate lowering of duodenal pH and contribute to duodenal ulcers
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45
Q

Crypts of Leiberkuhn

A
  • produce serous fluids that contains water and salts

- control of pancreatic secretions (secretin and CCK)

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46
Q

What stimulates the release of CCK by the small intestine

A

When fats are present in the duodenum

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47
Q

What causes release of bile salts into duodenum?

A

CCK stimulates contraction of the gall bladder which causes it to release bile salts

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48
Q

What is the purpose of bile salts?

A

emulsify fat

-increases the SA that pancreatic lipase can act

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49
Q

Segmenting contractions produced by the BER

A
  • most important when the small intestine is moving a meal
  • small segments contract and relax
  • moves contents up and down within small intestine
  • mixes content and maximizes contact with absorptive cells
  • 12X/min in duodenum
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50
Q

Peristalsis

A

dominates between meals

-moves stuff in small intestine distally to avoid stasis of contents

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51
Q

Gastro-Ileal reflex

A
  • when the stomach is active there is gastrin secretion, distention and gastric motility
  • this causes distal small intestine to move contents to colon to make room for new
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52
Q

Absorption of protein in small intestine

A
  • gastric, pancreatic, brush border enzymes perform digestion
  • actively transport with Na+ or via facilitated diffusion
  • absorbed into blood capillaries and transported to liver via portal system
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53
Q

Absorption of CHO in small intestine

A
  • digestion via salivary, pancreatic, brush border enzymes
  • actively transport with Na+ or via facilitated diffusion
  • absorbed into blood capillaries and transported to liver via portal system
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54
Q

Absorption of fat in small intestine

A
  • digestion primarily via pancreatic lipases, small contribution from salivary enzymes
  • chylomicron synthesis in intestinal absorptive cells
  • into lacteals and venous drainage into heart via lacteals
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55
Q

What is left in GI contents when it reaches the large intestine

A

-undigestible fiber, with some water and salts that were not absorbed in small intestine

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56
Q

Haustra

A
  • puckers in the longitudinal muscle layer of the large intestine
  • haustral churning is a major source of motility
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57
Q

Gastro-Colic reflex

A
  • intense sustained contraction of 15-20cm of colon
  • food in the stomach increases gastric motility and gastrin production
  • this reflex stimulates mass movement in the colon
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58
Q

Defecation reflex

A
  • stimulated by stretch of rectal smooth muscle
  • afferents in rectal wall convey stretch info to sacral segments in SC
  • parasymp efferents stimulate contraction of rectal smooth muscle
  • internal anal sphincter must relax
  • conscious control of relaxation of external sphincter then you poop
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59
Q

Irritable Bowel Syndrome

A
  • chronic disorder characterized by abdominal pain and altered bowel habits in the absence of pathology
  • more common in women (50% under 35 y/o)
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60
Q

IBS symptoms

A
  • recurrent abdominal pain for at least 3 days/month for 3 months
  • more or less bowel movements
  • pooping makes you better
  • any different type of stool
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61
Q

IBS treatment

A
  • stress management
  • avoid caffeine, lactose
  • anti diarrhea’s
  • tricyclic antidepressants
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62
Q

Inflammatory Bowel Disease

A

-Ulcerative colitis and Crohn disease

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63
Q

Crohn Disease

A
  • may involve entire length of GI tract but proximal is rare
  • ileum and cecum are common
  • non specific granulomatous inflammatory process (skip lesions)
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64
Q

Crohn treatment

A
  • avoid caffeine, spicy foods
  • drugs
  • corticosteroids
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65
Q

Ulcerative Colitis

A
  • always originates in rectum, can progress proximally

- mucosal lesions that produce regions of ulceration and necrosis

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66
Q

Ulcerative colitis symptoms

A
  • nausea, vomiting,
  • abdominal pain
  • rectal bleeding
  • diarrhea
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67
Q

Rotovirus

A

-common in infants and kids-
fecal oral transmission
-poor absorption so diarrhea

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68
Q

Diverticular disease

A
  • mucosal layer herniates through muscular layer forming a pouch
  • low fiber diet is risk factor
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69
Q

Diverticulitis

A

-inflammation of diverticulum

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70
Q

Diarrhea treatment

A

-bananas
-rice
-applesauce
-toast
BRAT

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71
Q

What are the Renal functions (7)

A
  • control extracellular fluid volume and osmolarity
  • excrete metabolic wastes toxins and drugs
  • synthesize hormones
  • control ECF concentration of ions
  • maintain the extracellular environment to keep cells functioning normally
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72
Q

How does the renal system regulate ECF volume

A
  • controlling amount of NaCl in ECF

- amount of ingested NaCl that is retained vs excreted

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73
Q

How does the renal system regulate ECF osmolarity

A
  • controls amount of ingested or synthesized water that is retained vs excreted
  • add water ECF becomes dilute, remove water ECF becomes concentrated
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74
Q

Filtration

A
  • the movement of water due to differences in hydrostatic pressure
  • important in determining the movement of H2O between vascular and interstitial spaces
  • not important in moving H2O between ICF and ECF
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75
Q

Osmosis

A
  • important in moving H2O in and out of capillaries

- only factor that determines whether H2O moves into or out of cells

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76
Q

What is the average osmolarity of a human cell

A

300mOsm

-hypo= 300

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77
Q

If a cell is in a hypertonic solution it will ___

A

-shrink

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78
Q

If a cell is in a hypotonic solution it will ___

A

-swell

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79
Q

Lower than normal plasma

A
  • pathology that prevents NA+ from being reabsorbed by the kidneys, individual loses more salt than water
  • ECF gets smaller
  • osmolatiry of ECF is lower
  • cells swell
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80
Q

Where does urine collect in the kidney

A
  • renal pelvis

- once urine reaches the renal pelvis it is not further modified

81
Q

Nephron

A

-a tube lined with a single layer of epithelial cells that are sitting on a basement membrane

82
Q

Artery flowing to the nephron is called the?

A

afferent arteriole

83
Q

Glomerulus

A

-tufts of capillaries in bowman capsule

84
Q

How much of the plasma in the afferent arteriole is filtered out into bowman space

A
  • 20%

- the other 80% exits the nephron via the efferent arteriole

85
Q

What does the loop of henle do?

A

communicates with the afferent arteriole to control blood flow

86
Q

What is after the loop of henle

A

-distal convoluted tubule

87
Q

Kidney filtration

A
  • plasma into bowmans space is 180 liters per day

- looks like plasma in afferent arteriole

88
Q

How is tubular fluid modified in the nephron

A
  • tubular secretion

- tubular reabsorption

89
Q

describe tubular secretion in the nephron

A

-the kidneys add solute to tubular fluid from the peritubular capillary network

90
Q

Describe Tubular reabsorption in the nephron

A
  • the movement of water and solute from the tubular fluid into the peritubular capillaries
  • major process of modification of tubular fluid
91
Q

What is different between systemic and renal capillaries

A
  • starling forces (large hydrostatic pressure pushing plasma into bowman space that remains high along length of capillary)
  • filtration barrier (glomerular caps are leaky
92
Q

Transport maximum

A
  • when transporters are saturated you get a further increase in solute concentration
  • not all glucose appears in urine until transport maximum is reached
93
Q

Plasma creatinine is proportional to _____

A

the number of function nephrons

94
Q

What does the proximal nephron do?

A

-reabsorbs 67% of all filtered solutes and water except glucose and AA (b/c they are all reabsorbed)

95
Q

In the proximal nephron reabsorptive functions are ______ homeostatic with respect to salt and water balance

A
  • NOT

- 67% of water and solute will be reabsorbed regardless of ECF volume and osmolarity

96
Q

What does the loop of Henle reabsorb

A
  • 15% of filtered water

- 25% of filtered solute

97
Q

What is preferential solute reabsorption

A
  • when more solute than water is reabsorbed

- occurs in the LOH

98
Q

Difference between ascending and descending limb

A
  • ascending is impermeable to water
  • decending is permeable to both salt and water
  • this creates a gradient that allows for concentration of urine
99
Q

Without ADH…..

A

-water is not reabsorbed in the distal nephron

100
Q

What does ADH do?

A

the hormone that homeostatically regulates distal nephron water reabsorption

101
Q

Excess water consumption does what to ECF osmolarity

A
  • decreases

- which is sensed by osmo-receptors that stops production of ADH

102
Q

What hormone controls distal nephron sodium reabsorption

A

-aldosterone, increases in this will increase sodium reabsorption in distal nephron

103
Q

Normal pH levels

A

7.35-7.45
lower is acidosis
higher is alkalosis

104
Q

What happens in ECF when [H+] is high

A

H+ moves into cells and K+ moves out causing hyperkalemia which depresses excitability

105
Q

Acid

A

hydrogen ion donor

106
Q

Base

A

hydrogen ion acceptor, takes hydrogen ions out of solution

107
Q

Chemical buffer

A

minimizes pH changes in the presence of an acid or alkaline load very rapidly

108
Q

What are the 3 systems that regulate plasma pH

A
  • chemical buffers
  • the lungs due to ability to control CO2
  • kidneys due to ability to reabsorb HCO3 and secrete H+
109
Q

Buffer systems

A

-have an acid component that will liberate H+ ions in solution when presented with an alkaline load and a base component that will remove H+ ions when challenged with an acid load

110
Q

Henderson Hasselbeck equation

A

pH= pKa + log [base]/[acid]

111
Q

Effectiveness of a buffer system

A
  • based on the [ ] of the buffers, higher [ ] gives the buffer system a greater capacity to minimize pH changes
  • the Ka, you want pKa near the desired pH
112
Q

Metabolic acidosis

A
  • pH is too low because [HCO3] is too low

- due to addition of fixed acids or loss of HCO3 like GI secretions

113
Q

Metabolic acidosis response

A
  • hyperventilate to decrease PCO2

- kidneys will reabsorb filtered HCO3 and secrete new HCO3 (takes hours to days)

114
Q

Causes of metabolic acidosis

A
  • production of fixed acids like lactate or ketoacids
  • decreased ability of the kidney to reabsorb bicarbonate or secrete H+
  • excessive loss of bicarbonate (diarrhea)
115
Q

Symptoms of metabolic acidosis

A

hyperventilation

-decreased nervous system activity

116
Q

Metabolic alkalosis

A
  • pH is too high because HCO3 is too high

- due to addition of alkali or loss of H+ (vomiting_

117
Q

Metabolic alkalosis response

A

-buffering by acid
-hypoventilation to increase PCO2
-kidneys will stop synthesizing HCO3 and stop reabsorbing HCO3
-

118
Q

Causes of metabolic alkalosis

A
  • much less common
  • excessive alkali ingestion (antacids)
  • chronic vomiting
  • hypokalemia
119
Q

Symptoms of metabolic alkalosis

A
  • hypoventilation

- excitation of NS function (seizures)

120
Q

Respiratory Acidosis

A
  • pH is too low because PCO2 is too high

- caused by decrease in alveolar ventilation

121
Q

Respiratory Acidosis response

A
  • chemical buffers do not play role
  • kidneys must reabsorb all filtered HCO3 and further synthesize new HCO3 to bring carbonic anhydrase equation back to the left
122
Q

Causes of respiratory acidosis

A
  • hypoventilation due to lung disease

- depression of respiratory centers

123
Q

Symptoms of respiratory acidosis

A
  • shortness of breath

- headache, blurred vision

124
Q

Respiratory alkalosis

A
  • pH is too high because PCO2 is too low

- not as common as resp. acidosis

125
Q

Respiratory alkalosis response

A

-kidneys decrease HCO3 and stop synthesizing HCO3

126
Q

Causes of respiratory alkalosis

A
  • hyperventilation due to anxiety or panic attacks
  • fever
  • altitude
127
Q

Symptoms of respiratory alkalosis

A

-hyperexcitability of CNS

128
Q

Base excess/deficit

A

the amount of HCO3 that must be added or removed from blood to achieve a pH of 7.4

  • positive = alkalosis
  • negative = acidosis
129
Q

Should protein/blood be present in urine

A

-no

130
Q

What is the normal pH range for urine

A

5.5-8.0 or greater

131
Q

What are the primary blood tests to evaluate kidney function

A
  • blood urea nitrogen

- creatinine

132
Q

What is GFR

A
  • glomerular filtration rate

- indicates the number of functional nephrons in the kidney

133
Q

Normal plasma creatinine levels

A
  1. 0 mg/dl

- if GFR is 50% of normal this value will double to 2.0

134
Q

Blood urea nitrogen (BUN)

A
  • normal value 8-20 mg/dl
  • increase in BUN indicates decrease in GFR
  • 2/3 of renal function can be lost before BUN increases
135
Q

What factors can affect BUN

A
  • increased dietary protein
  • GI bleeding
  • dehydration
136
Q

What 3 ways can diuretics act?

A
  • add non reabsorb able solute to tubular fluid to decrease gradient for distal reabsorption in distal nephron
  • inhibit solute reabsorption which also decreases H20 reabsorption
  • inhibit the release or action of ADH
137
Q

Osmotic diuretic

A
  • mannitol
  • reduce intracellular H2O volume
  • decrease intracranial pressure
138
Q

Carbonic Anhydrase inhibitor

A
  • acetazolamide
  • inhibits NaHCO3 reabsorption
  • can produce acidosis
  • treat mountain sickness
139
Q

Loop diuretics

A
  • furosemide
  • affect co transporter in loop of hence
  • most potent diuretics
140
Q

Thiazide diuretic

A
  • inhibits NaCl transporter at luminal membrane

- hydrochlorothiazide

141
Q

ADH antagonist

A

-treats hypertension/hyponatremia

142
Q

Kidney stones

A
  • damage can occur by urine stasis or increased pressure in urine tract
  • Nephrolithiasis
143
Q

Symptoms of kidney stones

A

-pain with location based on location of stone

144
Q

Kidney stone treatment

A
  • increase fluid intake
  • pain relief
  • avoid high oxalate foods
145
Q

Glomerulonephritis

A
  • inflammation and injury to glomeruli

- due to immune system attack

146
Q

What are the symptoms of glomerulonephritis

A
  • oliguiria
  • proteinuria
  • hematuiria
  • azotemia
  • hypertension
147
Q

Nephrotic syndrome

A
  • noninflammatory of golumerular cells causing gross proteinuria
  • hyperlipidemia
148
Q

Wilm’s tumor

A
  • pediatric

- tumor of genitourinary tract

149
Q

Causes of acute renal failure

A
  • decreased renal blood flow from shock
  • obstruction of urine outflow
  • acute tubular necrosis
150
Q

End Stage Renal Disease

A
151
Q

Exercise concerns for patients with chronic kidney disease

A
  • low CV fitness
  • generalized weakness
  • hypertension
152
Q

What type of cells line the ureter and bladder?

A

transitional epithelium

153
Q

Detrusor muscle

A
  • when it contracts urine leaves the bladder
  • internal urinary sphincter opens
  • when bladder is released it prevents urine from leaving bladder
154
Q

Female vs male urethra

A

-females are more prone to incontinence because there is less resistance to flow of urine

155
Q

Excitatory input causing bladder emptying is ______

A

parasympathetic

156
Q

Sympathetic input ______ bladder

A

relaxes

157
Q

Pelvic nerve carries _____

A

sensory info from stretch receptors in bladder wlal

158
Q

Pudendal nerve carries

A

sensory from external sphincter and pelvic muscles

159
Q

Micturition reflex

A
  • creates micturition waves that increase pressure and make you want to pee
  • contraction of bladder activates stretch receptors which continues contraction
160
Q

Anticholinergic

A
  • block receptors that cause detrusor contraction

- decreased tone

161
Q

Stress incontinence

A
  • involuntary leakage on effort or exertion

- women under 60

162
Q

Mixed incontinence

A

-involuntary leaking and urgency with effort

163
Q

Overflow incontinence

A

-bladder too full beacuse it cannot empty

164
Q

Functional incontinence

A
  • cannot get to place to piss

- caused by mobility loss

165
Q

UTI risk factors

A
  • sexually active
  • post menopausal
  • obstruction
  • diabetes
166
Q

Washout phenomenon

A

-urine coming out flushes out bacteria

167
Q

Pyelonephritis

A

ascending infection of urinary tract

-fever chills

168
Q

What is the most common sign of bladder cancer?

A

painless hematuria

169
Q

3 functions of the skin

A
  • protection
  • prevents loss of fluid
  • synthesis of vitamin D
170
Q

Stratum Germinativum

A
  • deepest and single layer of keratinocytes

- cells travel upwards

171
Q

Stratum Spinosum

A

2-4 layers thick and cells merge to form prickle cells

172
Q

Stratum Granulosum

A

3-5 layers of flattened keratinocytes

-dark granules containing keratohyalin

173
Q

Stratum Lucidum

A

-thin transparent layer found in hands and feet

174
Q

Stratum Corneum

A
  • multiple layers of dead keratinized cells

- 15-100 layers thick

175
Q

Melanocyte

A
  • dendritic cell producing melanin

- darker skin contains larger melanin with melanosomes

176
Q

Langerhans cells

A
  • antigen presenting dendritic cell from bone marrow

- important role in immune system

177
Q

Merkel cells

A
  • cutaneous sensation

- incresaed in hands for acute sensory perception

178
Q

Dermis

A

connective tissue layer with primary nutrition source for epidermis
-made of immune cells blood vessels

179
Q

Basement membrane zone

A

-interface between epidermis and dermis

180
Q

Macule

A

small flat

  • less than 1.0cm
  • freckle
181
Q

Patch

A

larger than 1.0 cm, change in color

-vitiligo

182
Q

Papule

A

elevated superficial up to 1.0cm

-elevated nevis

183
Q

Plaque

A

elevated superficial > 1.0cm

-expanding papule

184
Q

Wheal

A

irregular transient superficial edema

-mosquito bite

185
Q

Nodule

A

solid marble like >.5cm deeper and firmer than papule

186
Q

Vesicle

A

up to 1.0 cm filled with serous fluid

-herpes

187
Q

Bulla

A

> 1.0cm filled with serous fluid

-2nd degree burn

188
Q

Pustula

A

pus filled

-acne

189
Q

Ulcer

A

loss of epidermis and papillary dermis or subcutaneous tissue
-decubitous ulcer

190
Q

Callus

A

hyperkeratotic plaque of skin

191
Q

Corns

A
  • small circumscribed keratinous thickenings of skin

- corn on toes hands

192
Q

Albinism

A

-genetic disorder with partial absence of pigment in skin

193
Q

Vitiligo

A

-sudden appearance of white macule on skin

194
Q

Pruritus

A

-unpleasant sensation of itch leading to scratch

195
Q

Xerosis

A

-composition of gland secretion and decrease sweating

196
Q

Impetigo

A
  • superficial bacteria caused by staph common in infants and kids
  • small vesicle or large bulla
197
Q

Herpes simplex

A

-infections of skin

198
Q

Risk factors for skin ulcers

A
  • impaired sensation
  • skim moisture
  • incontinence
199
Q

Factors affecting wound healing

A

-nutritional status
blood flow and O2 delivery
-impaired immune response

Bioscience 2 (2 decks)

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