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Nursing Level 2 > Patho Midterm Two > Flashcards

Patho Midterm Two Flashcards

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1
Q

How is O2 transported in the body?

A

O2 binds to Hbg sites (has preferential binding).

Dissolves in blood

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2
Q

What effect will giving more O2 to a person will 99% sats have?

A

No effect. Site are already at max capacity.

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3
Q

What is the normal PaO2?

A

80mmHg

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4
Q

What happens to PaO2 as HbO2 drops?

A

Decreases. O2 will preferentially bind to HgB. If it isn’t binding to HgB then it won’t stay in blood

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5
Q

What factors affect HbO2 binding? How do they affect?

A
  • pH - <7.4 saturation binding decreases
  • temp - Increasing temp decreases binding abilities
  • Diphosphoglycerate (DPG) increases presence decreases O2 binding
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6
Q

What is a Bohr shift?

A

Shift to the right of the O2 dissociation curve

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7
Q

How does DPG decrease O2 binding? What causes increased levels of DPG

A

DPG binds to Hbg instead of O2.

Increase temp, thyroid hormone, testosterone and epinephrine raise DPG

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8
Q

What is Meconium? How does it influence fetal ARDs?

A

Meconium is fetal feces; if it enters the amniotic fluid it can contaminate it. In late gestation, the baby starts fetal breathing movements (FBM)s which can draw amniotic fluid into the lungs. Contaminated fluid can cause inflammation leading to hyaline inflammatory disease

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9
Q

What is ARDS?

A

Acute Respiritory Distress syndrome

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10
Q

What is the pathophysiology of ARDS?

A

Foreign particles / substances enter the alveoli (soot, pollutants) causing injury to type I epithelial cells. Neutrophiles enter and release inflammatory mediators and proteolytic enzymes. Causes hyaline membrane disease (thickening of injured area). Thickened area + fluid in alveoli = decreased diffusion in the area

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11
Q

What is hyaline membrane disease?

A

Inflammation of the basment membrane where damage to the epithelium was. Causes exposed basement membrane to thicken = decreased diffusion

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12
Q

What are manifestations of ARDS? Clinical consequences?

A

Manifestations:

  1. Leaky capillaries which lead to non cardiogenic edema
  2. Destruction of Type II alveoli cells causing atelectaisis
  3. Inflammation dt injury which causes fibrosis

Results in increased WOB, shunting (with alveoli collapsed, blood gets shunted elsewhere), hypoxemia

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13
Q

What is noncardiogenic pulmonary edema?

A

Pulmonary edema dt non CHF reasons (exudate following WBCs into lung)

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14
Q

What is patho cystic fibrosis?

A

Recessive disorder in individuals lacking the Cystic fibrosis transport regulator (CFTR) which causes a decrease in transport of Cl- watery solution. Without this solution the mucous sticks to the cillia in the bronchials..

The mucous forms a culture medium for bacteria growth causing recurrent infections

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15
Q

What are ways to management of CF?

A

Gene therapy, lung transplant, patthing person on the back, suctioning

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16
Q

What body parts does CF affect? What are possible S&S?

A

Respiritory: decreased air conductance

Pancreatic and bilary ducts: digestive problems, flatulence, steatorrhea, weight loss

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17
Q

What micro-organisms can cause respiritory tract infections?

A

Bacteria, viruses, mycosis, mycoplasma

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18
Q

What is typical pneumonia?

A

aka alveolae pneumonias. Dt bacteria

Infection attracts PMNs into alveolar lumen which produces exudate. Exudate causes respiritory distress

Cap endothelium breaks causing RBCs to enter alveoli - blood in sputum

Likely to have productive cough

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19
Q

What is atypical pneumonia?

A

aka interstitial pneumonia dt viruses

Alveoli lumen is clear. WBC enter alveoli walls though blood vessels. Edema builds up in walls

Increased thickness of walls decreases diffusion

Produces non productive cough

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20
Q

Differences between alveolar and interstitial pneumonias?

A

Alveolar

  1. fluid is in the alveoli
  2. RBC + WBCs in alveoli
  3. Productive bloody cough
  4. caused by bacteria

Interstitial:

  1. fluid is in interstitial walls
  2. alveoli lumen are clear
  3. non productive cough
  4. caused by viruses
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21
Q

What is bronchopneumonia? S&S?

A

Patchy distribution throughout both lungs. Diffuse.

S&S: Chills, fever, increased peripheral resistances, increased resp rate, bronchial breathing (gas exchange in the bronchi), purulent and bloody sputum. Severe chest pain and abdominal distension)

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22
Q

What is lobar pneumonia? what are clinical manifestations?

A

Pneumonia in one lobe of lung. All the alveoli are infected. Associated with consolidation of lobe.

S&S: Shallow breathing, cyanosis, pleurisy (pleuritis), N&V, rust colored sputum, fever, chills

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23
Q

What is interstitial pnemonia? Clinical manifestiation?

A

Widespread disttribution. Diffuse inflammation dt viral infeciton. Walls are inflitrated with WBCs which increase septum width

S&S: cyanosis, fever, chills, alveolar wall fibrosis, non productive cough, finger clubbing (severe)

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24
Q

Why is the right lower lobe most often implicated with lobar pneumonia?

A

Rt bronchus is more vertical dt the position of the heart than the lt bronchus. Makes Pathogens more likely to enter and settle

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25
Q

What is the pathogenesis of clubbing fingers?

A

May be an immune response dt the lack of O2 supply

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26
Q

What is prostration?

A

extreme weakness and fatigue

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27
Q

Why is the sputum rusty colored in lobar pneumonia?

A

Caused by inflammation and destruction of tissue

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28
Q

What are complications of pneumonia?

A
  1. Pleural fibrosis dt chronic inflammation in lungs
  2. Empyema - decreases ventilation bc of increase of resistance
  3. abcess - mass loss of tissue in lung - decreases lung capacity
  4. Bronchiectasis - bronchi are permanently enlarged. Increases air deaad space which means less air to the alveoli
  5. Intersitial fibrosis
  6. Cysts - fluid filled sacs which destroy alveoli
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29
Q

What is TB? Where is it most proliferative?

A

Infectoius agent that causes the most deaths

Mostly in developing countries

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30
Q

What are characteristics of Mycobacterium tuberculosis hominis?

A

T bacteria -

Aerobic, has a protective waxy capsule which allows it to say alive in “suspended animation for years.

Usually affect superior lobes

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31
Q

How long does it take after initial infection for the TB test to read positive?

A

3-6 weeks

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32
Q

What is the Ghon complex?

A

Encapsulated nodes in the lung lobes which encloses TB to prevent further spread

Contains Macrophages, T cells and inactive TB bacteria

Visible on xrays, partially dt dystrophic calcification of necrotic areas

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33
Q

What is the immune mediated response of initial TB infection?

A

Bacteria is inhaled.

Macrophages ingest bacteria and present the infectious agents on outside.

T cells are activated to kill macrophages with bacteria inside and also activate macrophages to target TB more efficiently

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34
Q

What is primary TB?

A

If the immune response is adequate, TB trapped in Ghon foci. Bacteria are rendered inactive and non contagious

If the immune system is weak (Elderly, AIDs) the bacteria multiply in lungs. aka progressively primary TB. These individuals are contagious.

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35
Q

What is Milary TB?

A

Second phase of TB after Progressive primary TB.

Pt exhibits signs of pneumonia (dt WBC activation), bacteria in sputum and exhaled droplets. TB bacteria can spread to the rest of the body - brain, bone, gonads, urinary tract, GI, heart and adrenal glands

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36
Q

What is secondary TB?

A

When a person is reinfected with TB which causes reactivation of previously healed lesion

Body can respond quicker

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37
Q

What is consumption?

A

Creation of cavities in lungs dt untreated TB

Can be fatal

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38
Q

What is potential space?

A

Free space in the abdomen to allow for movement and expansion of the organs

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39
Q

Different between parietal and visceral peritoneum

A

Parietal lines abdominal cavity, visceral lines organs

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40
Q

What separates the mucosa and submucosa>

A

muscalaris mucosa

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41
Q

What are the functions of saliva?

A

Improves taste of food by dissolving foods

Starts the digestion process

Protects the mouth from infectious agents

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42
Q

What are the different salivary glands?

A

Parotid: Produces most of the salivary fluid. Serous, watery fluid

Sublingual: Smallest, secretes mucous

Submandibular - secretes serous and mucous

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43
Q

What muscles are found in the esophagus?

A

Upper 1/3 - skeletal. Gag reflex present

Lower 2/3 - smooth muscles - peristalsis

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44
Q

Why does heart burn occur?

A

Weakness in diaphragm muscles (around cardiac sphincter) are weak.

When the stomach moves around, acid splashed back and enters the esophagus

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45
Q

What are the stagse of swallowing?

A

Buccal Phase: Food is turned into a bolus. Tongue moves bolus to the back of the throat towards the esophaugs

Epiglotis covers trachea.

Pharyngeal - esophageal phase: Upper 1/3, pt can regurgitate

Lower 2/3 peristalsis. Moves towards cardiac sphincer

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46
Q

Why does the stomach have three layers of smooth muscle?

A

To chop food and mix digestive juices

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47
Q

Label the following:

A
  1. Fundus
  2. Cardiac region
  3. Body
  4. Longitudinal muscle
  5. Circular muscle layer
  6. Oblique muscle
  7. Gastric rugae
  8. Antrum
  9. Pyloric canal
  10. Pylorus
  11. Pyloric sphincter
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48
Q

What is the stomach Ph?

A

1-2

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49
Q

What are the major secretory cells of the stomach? What do they produce?

A

Parietal cells - produce HCl & Intrinsic factor

Chief cells - granules secrete digestive enzymes (pepsinogen)

Enteroendocrine - secrete hormones into the blood

Surface epithelia - HCO2 & mucous

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50
Q

How is hCl formed?

A

CO2 in blood is converted to carbonic anahydrase in the parietal cells. It is broken up into HCO3 (which re-enters the blood) and H+ ions, which are secreted into the stomach lumen

Chloride is pumped from the blood stream

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51
Q

What medications stop the hydrogen ion pump?

A

Pantoloc - inhibits H+K+ATPase. Prevents the release of H ions

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52
Q

What are the phases of HCL secretion?

A
  1. Cephalic: Thought of food stimulates the vagus nerve which causes the release of HCl
  2. Gastric: distension of the stomach causes the release of histamine and gastrin. This causes HCL release
  3. Intestinal: When food leaves the stomac, hCL is inhibied due to secretin, CCK and GIP
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53
Q

What does secretin do?

A

Releases HCO3 to neutralize HCL

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54
Q

How do you control gastric secretions?

A
  1. Block Muscarinic receptor - block AcH, but not usually done because it can cause other problems
  2. Block H2 receptors by blocking histamines - treated with Zantac
  3. Block gastric receptors
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55
Q

What are the functions of HCL?

A
  1. Actuvates enzymes such as pepsin
  2. Breaks up connectoive tissue and plant walls liquifying into chyme
  3. Converts Ferrie ions +3 to ferrous ions +2 which can be absorbed and utilized for Hbg
  4. Destroys bacteria and pathogens
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56
Q

How is pepsinogen converted?

A

HCl cleaves pepsinogen into two particles which creates pepsin

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57
Q

What fluids are secreted in the small intestines? From where? Where to?

A

Pancrease into duodenum: HCO3, proteases, lipases amylases

Gallbladder to duodenum: Bile acids, pigments, phospholipids

Secretions from intestinal epithelia: brush border enzymes help digest carbs and proteins

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58
Q

What is zymogens?

A

inactivated proteins

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59
Q

What enzymes do are activated by brush border epithelium?

A

Trypsinogen to tripsin

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60
Q

When is CCK released? WHat does it cause? What happens if it is missing?

A

CCK = cholecystokinin

Released from duodenum when stomach acid and fat enter duodenum

Causes the contraction of the gallbladder, secretion of pancreatic enzymes and relaxation of hepatopancreatic sphincter

If lacking, bile not released, fats not emulsified = fatty stool (steatorrhea). Can be a temporary condition

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61
Q

What causes secretin to be released? WHere does this happen? What happens when secretin is released.

A

Released when chyme released in duodenum, Stimulates all ducts to release bicarbonate

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62
Q

What happens when an enzyme for digestion is missing?

A

Inaqequate digestion leads to inadequate absorption which leads to malabsorption syndrome

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63
Q

Where does most of the disgestion occur?

A

In the duodenum - where most of the catalyzing enzymes are put

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64
Q

When a patient is dehydrated, why are they given solutions of glucose + electrolytes(pedialite)?

A

In the small intesting, Glucose and Na+ are transported together from the blood to the intestine. If one is missing, the transport won’t occur.

If just electrolytes are given orally, gut can become hypertonic, drawing fluid from the blood stream, exacerbating the dehydration

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65
Q

What is the process of fat digestion?

A

Large fat globules are broken down by Lethcin and bile acids (decreased SA = easier digestion)

Broken into free fatty acids x2, mono glyceride

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66
Q

What’s the role of the illeocecal valve?

A

Regulates the entrance of chyme into large intestine

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67
Q

WHere does H2O absorption occur in GI tract?

A

Sm Intesting - absorbs 90% H2O

Lrg intestine - absorbs some

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68
Q

Histiological diffferences between small and large intestine?

A
  1. Small intestine
    : microvilli & circular folds for increased absoprtion abilities

produce some digestive enzymes

2: Large intestine:

Simple columnar epithelium, intestinal crypts to produce mucous, haustra to compact feces

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69
Q

What are the function of the cells found in the large intestine?

A
  1. Peyes patches: clean up infections
  2. Goblet cells produce mucous to facilitate fecal movement

Haustra: compact feces by removing H2O

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70
Q

What are the functions of smooth muscle movements in the GI tracy (Gastric motility)

A
  1. Mixed chyme with intestinal, bile and pancreatic secretions
  2. Churns chyme to increase contact with mucosa for absoprtion
  3. Moves residue towards large intestine
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71
Q

What is the difference between segmentation and peristalsis?

A

Segmentation: Random ringlike constrictions which mixes and churns contents. Occurs ~12/min in duod

Peristalsis: Wave like contractions that pushes food down. Controlled by migrating motor complex

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72
Q

Difference between small and large bowel motility?

A

Small: Takes 2-4hrs to transverse. Segmental and peristaltic movements

Large- segmental contractions make haustra

1-3 mass movements/day

73
Q

What is the nerve/ motor movements of defecation?

A

Filling of rectum activates nerve endings. Carried to spinal cord, which activates motor neurons causing the internal anal sphincter (smooth muscle) to relax.

Voluntary relaxation of the muscle is controlled by impulses directed from brain. Relaxation of external sphincter and compression of abdo muscles

74
Q

What causes dysphagia?

A

Neuromuscular dysfunction (Oropharyngeal phase)

Stricture/ tumor

Esophageal motility disorder

75
Q

What are the features of oropharyngeal dysphagia?

A
  • nasal regurgitation (improper closing of uvula)
  • Airway obstruction during eating (abnormal epiglottis function
  • Coughing when swallowing
  • Immediate regurgitation
  • Horse voice dt food stuck in larynx
76
Q

Featuresof esophageal dysphagia?

A
  • No airway distress
  • Late regurgitation
  • Chest pain at meals
  • Frequent heart burn
  • Swelling of left supraclavicular LN
77
Q

What is achalasia? What are S&S? How is it treated?

A

Stenosis of the esophagus dt poor relaxation of the lower esophageal sphincter. Not understood what causes it. Pt feels chest pain and regurgitation. LES can be loosened surgically

78
Q

What is a hiatal hernia?

A

Stomach moves in three directions which causes the stomach to piece through the diaphragm (hiatal hernia)

79
Q

What is esophagitis?

A

Inflammation of the esophagus dt gastric acid reflux and often associated with hiatal hernia

80
Q

Who does esophagitis affect?

A

Individuals over 40, obese

81
Q

What is Barratts esophagus?

A

Metaplasia of stratified squamous epithelia changed to acid secreting columnar cell

Increased risk of esphageal cancer

82
Q

What is Mallory Weiss syndrome?

A

a tear in the esophageal membrane leading to bleeding and emesis. May be dt chronic GERD or hiatal hernia

83
Q

WHat is acute gastritis? What causes it?

A

Transient inflammation of the stomach mucosa resulting in hemorrhage. (acid hypersecretion)

Unknown. May be related to aspirin & NSAIDs, alcohol abuse, heavy smoking, stress, shock, erythromycin

84
Q

Why do NSAIDs cause acute gastritis?

A

Thought to decrease mucous protection in gastric mucosa

85
Q

What are pathological characteristics of acute gastritis?

A

hyperemia, superficial erosions and ulcerations.

Erosions of blood vessels are several and small

86
Q

Signs and symptoms of acute gastritis?

A

Intense pain with stomach emptying (in am)

87
Q

What causes chronic gastritis? Where in the stomach is it generally found and why?

A

Main type of gastritis, usually related to H pylori or autoimmune responses

Most commonly found in pylorus (may be dt pyloric sphincter fibrosis and back flush)

88
Q

Why is pernicious anemia associated with chronic gastritis?

A

hyperacid secretion causes decreased production of intrinsic factor

leads to B12 deficiency

leads to decreased Hgb production

89
Q

How long does it take for food to pass through the duodenum

A

2hrs

90
Q

Where are peptic ulcers generally found?

A

duodenum mostly

91
Q

What are the pathological features of chronic gastritis?

A

Pale, atrophic mucosa

Recurrent, deep and solitary

92
Q

What are features of peptic ulcers?

A

Round, sharply demarcated pit a few centimeters in diamter

ulcerated through mucosa and submucosa

presence of granulation tissue

bleeding of erroded blood vessels

93
Q

What is the most dangerous complication of peptic ulcer

A

Perforation of the GI wall - bacteria from GI enters the blood stream causing septic shock

94
Q

What is enterocolitis?

A

Inflammation of small and large intestine, characterized by diarrhea

95
Q

What is the pathogenesis of enterocolitis?

A

An infectious material is ingested

Infection produces a mild bowel inflammation which is an attempt to get rid of the agent

Inflammatory exudate is produced to dilute toxins

Volume expansion causes increased stretch which increases bowel motility - N&V , diarrhea

Decreased digestive enzymes from brush border = less food absorption, food passess through. Draws H2O from bowel causing electrolyte disruption

96
Q

What are the differences of diarrhea caused by small and large intestine.

A

Small: Large volume, watery appearance, rare frank blood, pain in periumbelical atrea

Large: Small amount, mucoid appearance, common to have frank blood, pain in LLQ area

97
Q

What is ulcerative colitis? What are signs and symptoms?

A

An inflammatory bowel disease which involves only the colon and the rectum (most of inflammation is in anus and rectosigmoid area)

Only affects superficial mucosa

Inflammation in continous area

Bloody diarrhea and lower abdominal cramps

98
Q

What are pathological features of ulcerative colitis?

A

Mucosal involvement - no involvement in or below smooth muscle

Broad, superficial ulcers leaving polypoid islands of inflammed intestinal

Intestinal wall remains same width

99
Q

What are complications of ulcerative colitis?

A

Megacolon, erythema nodosum, arthritis, malnutrition, sclerosis cholangitis, increased cancer risk

100
Q

WHat is megacolon?

A

Affected area becomes swollen. If due to bacteria = toxic megacolon.

Wall becomes thinner dt swelling and may perforate

101
Q

What is Crohns disease? What are features of the disease?

A

Systemic autoimmune disease causing inflammation of the whole GI tract.

Most common = terminal llem

Segmented inflammatory reaction

Involves the whole thickness of bowel wall

Inflammed segments are stiff and rubbery

102
Q

What are pathological features of crohns?

A

Lacks polypoid islands

Occult blood in stool

Inflammation throught whole wall

103
Q

What are clinical features of Crohns?

A

Intermittent bouts of fever and diarrhea (intermittent flare ups)

May have RLQ mass/ tenderness

Ulcerations, strictures and fistulas

Slightly elevated risk of ca (not as much as ulcerative colitis)

Arthritis, erythema nodosum, sclerosing cholangitis

104
Q

What are the similarities between crohns and ulcerative colitis?

A

Both are hereditary

Peak age of occurance: 15-25yrs

Has an autoimmune etiology

Have extraintestinal complications

Treated with corticosteriods to decrease freqency of episodes

105
Q

What are the differences between Crohns and Ulcerative colitis?

A

Crohns: Segmentative distribution in all GI tract

Has granulomas has fistulas

Megacolon does not occur

Some cancer risk

No polyps

Ulcerative Colitis: Continous distribution in Lrg intestine only

No granulomas or fistulas

Risk of megacolon

Increases cancer risk

Polyps ++

106
Q

What is diverticular disease?

A

Formation of outpouches on the large colon on the weak spots (haustra where arteries enter large intestine).

Happens predominantly in large intestine

Occurs in elderly, large protein and small fiber diets (increases pressure

107
Q

What is diverticulosis?

A

Presence of diverticular disease

108
Q

What is diverticulitis? How does it present?

A

When a diverticulum ruptures dt infection (fecal matter inside of outpouch)

Presents in eldery with LLQ pain, severe constipation dt colon constriction, nausea and fever

109
Q

What are complications of diverticulitis?

A
  1. Fecaliths
  2. Perforation
  3. Hemorrhage
  4. Abcess
  5. Fistula
  6. Stenosis dt fibrosis
  7. Colonic masses
110
Q

What is the difference between sterile and infectious peritonitis?

A

Sterile: When chemical reactions happen in the peritoneum. ie pancreatic proteases escape from pancreas and attack surrounding cells which causes inflammation

Infectious: When intestinal flora escape from the GI tract dt GI wall perforation or due to accumulation of ascites, a ruptured liver abcess or salpingitis

111
Q

What are some complications of peritonitis?

A

Purulent inflammatory exudate throughout the entire abdominal cavity

Formation of fibrinous lesions

sepsis

112
Q

What is the pathogenesis of appendicitis

A

fecalith obstructs the lumen of the appendix which blocks draining mucous

Increase pressure behind the obstruction which hinders blood flow

Edema, ischemia, necrosis and bacterial overgrowth

Can rupture and cause sepsis

113
Q

How does appendicitis present?

A

RLQ pain, N&V, fever, diarrhea,

114
Q

Depending on the part of the GI tract, what are S&S of GI hemorrhage?

A

Above stomach: Frank hematemesis

Hem in stomach: coffee grounds vomitus

Hem in Intestine: Occult fecal blood

Hem in lrg intestine/ lrg amounts of blood: Melena

Rectum: Red coated stool

115
Q

What causes mechanical obstruction? What are S&S?

A

From the twisting, compression or presence of blockage in the GI lumen

Manfestations: Severe, colicky pain

audible high pitched peristalsis - pt aware of intestinal movements

116
Q

What is colicky pain?

A

Spasmotic - goes in waves

117
Q

What is the difference between mechanical and paralytic obstruction

A

Mechanical: presence of BS

Paralytic: absence of BS

118
Q

What causes paralytic illeus?

A

Gastroenteritis, electrolyte balances, abdo surgery (especally on intestine), narcotics, anesthesia, spinal cord inury

119
Q

What are manifestations of illeus? How is it treated?

A

Manifestations: continuous pain, absences of BS, distended abdoment, dyspepsia (feeling of fullness), gas and constipations

Tx’d: ambulation, NG tubes, medications that induce peristalsis

120
Q

What are examples of mechanical obstructions?

A

Hernia, volvulus, intussusception, bowel tumor

121
Q

What is a hernia? How does it affect normal bowel function?

A

Hernia is a protrusion of the bowel through a weak part of the abdominal wall

Pressure on the GI wall can impair the venous blood flow, which causes edema. Can cause decreased blood flow to bowel and bowel death

122
Q

What is the most common site of hernias?

A

Inguinal canal in males. Not as comomon in females

123
Q

What is a volvulus? Where does it occur? What are results of a volvulus?

A

Volvulus is when the bowel twists on itself (often dt prolapsed mesentery)

Occurs in the illeum, cecum or signoid colon

Can lead to GI wall necrosis, peritonitis, pain and sepsis

124
Q

What is intussusception? Where does it occur?

A

When part of the intestine folds back over itsself

Most often occurs in terminal illeum

125
Q

What are pathological manifestiations? Clinical? Who does it often occuri n?

A

Patho: compression of messentery causing engorgment of veins, ischemia and bleeding, sepsis

Clinical: Pain, current jelly stol dt increases mucous secretions

Happens ideopathically in children 3mos - 6 years

126
Q

What can result dt a GI obstruction?

A
  • Vomitting leading to electrolyte imbalance
  • Fluids entering GI contents instead of blood stream
  • Gas accumulation
  • Distension of bowel
  • Compartment syndrome causing ischemia and or necrosis
  • GI bacteria produces endotoxin leading to toxemia
  • Malabsorption
127
Q

What is compartment syndrome:

A

lower area of bowel is cut off from nutrients. May cause ischemia

128
Q

What is a liver lobule?

A

Functional until of the liver

129
Q

What vessels are in the triad?

A

Hepatic artery, portal vein, and bile duct

130
Q

Where does the central vein drain to

A

Inf vena cava

131
Q

How much blood is delievered to the liver from the hepatic artery?

A

20%

132
Q

What are the functions of the liver?

A
  1. Nutrient metabolism (glucose to glycogen, lipids to triglycerides, lipid soluble vitamins) prepares for storage
  2. Production of serum enzymes and proteins (albumin, clotting factors)
  3. Drug and hormone metabolism- biotransformation to water soluble forms and detoxification and inactivation of drugs
  4. Urea synthesis - breaks down ammonia
  5. Bile synthesis
133
Q

What are RBCs broken down to?

A

unconjugated bilirubin - conjugated bilirubin (by liver) - bile

134
Q

What concentrations of bilirubin cause jaundice?

A

>3mg/dl

135
Q

What causes jaundice to occur?

A

Increased RBC breakdown

Impaired liver reuptake of bilirubin

Impaired excretion of bilirubin

136
Q

What is prehapatic jaundice?

A

caused by increased levels of unconjugated bilirubin in bloodm May be due to impaired breakdown on RBCs dt RBC disorders (polycythemia, sickle cell anemia), diseases which enlarge the spleen (mono)

blood bilirubin will be unconjugated

137
Q

What is hepatic jaundice?

A

Caused by interference of the liver’s ability to conjugate bilirubin or secrete it after conjugation dt a tumor, inflammation or cirrhosis

Blood bilirubin my be conjugated or unconjugated

138
Q

What is post hepatic jaundice?

A

Caused by the obstruction of flow outside of the liver. ie obstruction of the gall bladder (gallstones/bile duct obstruction). Bilirubin no excreted in feces

Increased conjugate levels of bilirubin

139
Q

In a urine sample, what is indirect bilirubin?

A
  • Bound to albumin so decreased bilirubin in urine (albumin too large to filter out of blood)
  • There is visible jaundice

unconjugated, associated with prehepatic jaundice

140
Q

What is direct bilirubin?

A

Conjugated bilirubin, not attached to albumin, so found in urine.

VIsible jaundice

141
Q

What is acute hepatitis? What causes it?

A

acute liver inflammation dt virus or hepatotoxins

142
Q

What are clnical manifestions of all the hepatitis?

A

Jaundice, hepatomegaly, fever, GI distress, fatigue, dark urine (from hemoglobinuria), anorexia, abdominal discomfort

143
Q

What is the transmission, risk and prognosis of Hep A

A

T: oral-fecal

R: Contaminated food

P: Good with robuse immune system

144
Q

What is the transmission, risk and prognosis of Hep B/D

A

T: Blood and body fluids

R: Sexual, IV

P: More severe, especially when B&D combined. Less acute SE than A, and less chronic than C

145
Q

Why is the prognosis poor when a patient has Hep B &D

A

They have similar manifestations and act synergistically

146
Q

What is the transmission, risk and prognosis of Hep C

A

T: Blood and body fluids

R: Sexual, IV

P: 85% chronic stage (insiduous onset)

147
Q

What is the transmission, risk and prognosis of Hep E

A

T: Oral-fecal

R: Water bourne

P: ?

148
Q

What tests are done to evaluate for acute hepatitis?

A

History of viral or toxin exposure

Presense of liver enzymes (ALT, AST)

Bilirubin levels

Coagulation tests

Plasma proteins

Serology for viral hepatitis

149
Q

What are examples of liver toxins?

A

Tylenol, alcohol

150
Q

Why are increased AST, ALT indicators of hepatitis?

A

Not normally found in blood unless liver cells have been damaged/ destroyed and they have leaked into the blood stream

151
Q

Is chronic hepatitis symptomatic?

A

May not be. Why severe damage can happen in those with Hep C… onset is insiduous and therefore a lot of damage can happen before S&S start

152
Q

How many people in the world have Hep B? What percentage are symptomatic.

How many cases of chronic carriers are there in Africa and Asia out of total cases

What percentage of acute symptomatic Hep B infection recover?

A
  1. 2B
  2. 35% symptomatic

320-350M/360M

90%

153
Q

With Hep C infection, What percent recover, what percent goes into chronic disease?

Of chronic, which % have cirrhosis

A

30-50% recover from an acute case

50-70% develop chronic disease

25-35% of those with chronic disease have cirrhosis

154
Q

What are the principle causes of chronic liver disease, cirrhosis and liver ca?

A

Hep B & C

155
Q

What is acute toxic hepatitis? How do you test for it?

A

exposure to a hepatotoxin or its metabolite

No definitive test - check hx of exposure, have negative serology screen, improvement after d/c of a drug

156
Q

What is the ratio of AST to ALT in alcohol poisening?

A

2:1

157
Q

What is alchol dehydrogenase?

A

Liver enzyme which breaks down alcohol. Activity of ADH varies among different individuals and ethnicities. Decreased ADH = decreased ability to break down alcohol = increase risk of developing chornic liver disease when person is a chronic drinker

158
Q

What percentage of alcoholics develop liver disease?

A

15-20%

159
Q

How does alcoholic liver disease present?

A
  1. Fatty liver (steatosis) - dt storage of triglycerides and deposition in liver. Causes liver to enlarge
  2. Alcoholic hepatitis - dt liver inflammation which causes necrosis and fibrosis
  3. Cirrhosis - scar tissue which partially blocks sinosoids and bile canaliculi
160
Q

What are Mallory bodies?

A

Damaged proteins which collect in liver

161
Q

WHat is the anatomic continuum of liver injury?

A
  1. Inflammation. Liver is normal sized and smooth
  2. Degeneration: Liver enlarges because of fatty deposits
  3. Necrosis
  4. Fibrosis - liver shrinks smaller than a normal liver, liver is nodular
162
Q

What are the causes of Cirrhosis

A

Main causes: Alcohol, Hepatitis virus

Other causes: Drugs, hereditary metabolic diseases (hemochromocytosis), autoimmune diseases (primary sclerosing cholangitis, autoimmune hepatitis), biliary obstruction

163
Q

What are the clinical features of cirrhosis?

A

Failure to metabolize estrogen and ammonia, protein synthesis failure, excretory failure, and portal hypertension

164
Q

What are S ans S of failure to metabolise estrogen and ammonia?

A

  1. Thinning of hair 2. Coma st increased levels of ammonia 3. Fetor hepaticus fecal smelling breath 4. Spider nevi (red patches on skin dt estrogen opening capillary sphincters) 5, Gynocomastia 6. Palmar erythema dt increased circulating estrogen 7. Reduced pubic hair 8. Smaller tesis
165
Q

What are signs and symptoms of protein synthesis failure?

A

  1. Ascites 2. Purpura 3. Edema
166
Q

What causes ascites?

A

Decreased production of albumn causes fluid to escapes into the abdominal cavity Portal HTN - the liver is too stiff to recieve blood therefore extra fluid enters abdo Hyperaldosteornism - Na retention causes H2O retention. Extra fluid not held by albumin and enters abdo cavity

167
Q

What causes purpura?

A

East bleedig dt increased estrogen which causes increased blood at the surface and a decrease of clotting factor

168
Q

What are s and S of excretiry failure?

A

Jaundice

169
Q

What are signs and symptoms of portal HTN?

A

  1. Splenomegaly 2. Collaterial veins 3. Ascites 4. Edema
170
Q

Why does spenomegaly occur?

A

Blood from the liver backs up in the spleen causing it to enlarge getting bigger than the liver

171
Q

what are collateral veins?

A

portal - systemic anatomoes form because its too difficult for blood to go through portal vein so they go through systemic veins instead the PV. Can cause hemorrhoids

172
Q

What is caput medusa?

A

distension of the umbelical vein

173
Q

What are manifestaions of cell failure in liver cirrhosis?

A

Jaundice Bleeding Low albumin Immune deficiency Estrogen deficiency (palmar erythema, gyncomastia, spider nevi) Encephalopathy

174
Q

Why vdoes cirrhosis cause encephalopathy?

A

increased ammonia affects CNS causing memory loss and movement disorders (astrixes)

175
Q

What are esophageal varices?

A

a sign of portal hypertension

176
Q

what is hepatorenal system?

A

cirrhosis causes decrease of blood flow to the kidneys less wastes are filtered Increase in BUN and creatinine

177
Q

What are abnormal lab findings related to cirrhosis?

A

Increase transaminases (ALT and AST) Decreased albumin Increased PTT Increased NH3

178
Q
A

Nursing Level 2 (6 decks)

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