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A&P III > GIT > Flashcards

GIT Flashcards

1
Q

Identify the source action and regulation of Intrinsic factor

A

From Parietal cells

Facilitates Vit B12 absorption

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2
Q

Identify the source action and regulation of Gastric acid

A

Parietal cells

Lowers pH to optimal range for pepsin function

Release is stimulated by histamine, Ach, gastrin
and inhibited by PG, somatostatin, GIP

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3
Q

Identify the source action and regulation of Pepsin

A

From Chief cells

Facilitates Protein digestion

Release is stimulated by vagal input and local acid

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4
Q

Identify the source action and regulation of Cholecystokinin (CCK)

A

From I cells of duodenum and jejunum

Increases GB contraction and Pancreatic secretion. Decreases gastric emptying.

Release is stimulated by increased presence of fatty acids and amino acids

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5
Q

Identify the source action and regulation of Cholecystokinin (CCK)

A

From I cells of duodenum and jejunum

Increases GB contraction and Pancreatic secretion. Decreases gastric emptying.

Release is stimulated by increased presence of fatty acids and amino acids/ monoglycerides in the duodenum

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6
Q

Identify the source action and regulation of Somatostatin

A

From D cells in pancreatic islets , GI mucosa

Inhibits release of ALL GI hormones

Release stimulated by acid and inhibited by vagus

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7
Q

In Cholelithiasis , pain worsen after eating fatty foods due to?

A

Increased secretion of Cholesystokinin

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8
Q

Alkaline pancreatic juice in duodenum neutralizes gastric acid, allowing pancreatic enzymes to function.

A

Secretin

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9
Q

Very inhibitory hormones- Anti GH

A

Somatostatin

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10
Q

This GI secretion is used to treat VIPomas and carcinoid tumors

A

Somatostatin

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11
Q

Destruction of this GI secretion will result in Pernicious anemia

A

Intrinsic factor

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12
Q

Inadequacy of this GI secretion predisposes to a high risk of Salmonella

A

Gastric Acid

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13
Q

Pesin by H+

A

Pepsinogen

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14
Q

This part of GI wall decreases diameter

A

Circular muscle (think circle)

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15
Q

This part of GI tract shortens a segment

A

Longitudinal muscle (think length)

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16
Q

Structure of the wall of GI tract

A

Epithelial cells- For secretion or absorption

Muscularis mucosa

Circular muscle- reduce diameter

Longitudinal muscle- shortening of a segment

Submucosal plexus (Meissner’s plexus and myenteric plexus)- Comprise the enteric nervous system, coordinate motility, secretory and endocrine functions of GIT

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17
Q

These cells of GI tract are responsible for absorption and secretion

A

Epithelial cells

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18
Q

This part of GI tract wall Comprise the enteric nervous system, coordinate motility, secretory and endocrine functions of GIT.

A

Submucosal plexus (Meissner’s plexus and myenteric plexus)

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19
Q

Describe the Intrinsic Innervation (enteric nervous system)

A

100 millions neurons

Coordinate information from PNS and SNS to GIT

Uses local reflexes to relay information within GIT

Controls most functions e.g. motility and secretion even in the absence of extrinsic innervation - “ Gut brain”

Myenteric plexus (Auerbach’s plexus)- Controls Motility

Submucosal plexus ( Meissner’s plexus)- Controls Secretion and blood flow

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20
Q

This Coordinates information from PNS and SNS to GIT and Uses local reflexes to relay information within GIT

A

Intrinsic Innervation (enteric nervous system)

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21
Q

Controls Motility

A

Myenteric plexus (Auerbach’s plexus)

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22
Q

Controls Secretion and blood flow

A

Submucosal plexus ( Meissner’s plexus)

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23
Q

Four “official” GI hormones are

A

gastrin
cholecystokinin (CCK)
secretin
glucose-dependent insulinotropic peptide (GIP).

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24
Q

GI hormones release from endocrine cells of GI mucosa into _________________, enter ________________ and have physiological actions on target tissues.

A

portal circulation

general circulation

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25
Q

Gastrin

A

Is released in response to meal from G cells of the gastric antrum.

Increases H+ secretion by gastric parietal cells and Stimulates growth of gastric mucosa – trophic action.

Release is stimulated by small peptides and amino acids esp. phenylalanine and tryptophan; Distension of stomach and; Vagal stimulation

Release is Inhibited by Acid [H+] in the lumen of stomach (-ve feedback)

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26
Q

Release of Gastrin is stimulated by?

A

Small peptides and amino acids esp. phenylalanine and tryptophan.

Distension of stomach

Vagal stimulation

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27
Q

Occurs when gastrin is secreted by non-beta-cells of pancreas resulting in hypertrophy of gastric mucosa

A

Zollinger-Ellison syndrome (gastrinoma)

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28
Q

What are the actions of Cholecystokinin (CCK)

A

Stimulates contraction of GB , relaxation of sphincter of Oddi leading to ejection of bile.

Stimulates pancreatic enzyme secretion.

Potentiate secretin-induced stimulation of pancreatic HCO3 secretion.

Stimulates growth of exocrine pancreas.

Inhibits gastric emptying. Thus fatty meal stimulates CCK, which slows gastric emptying. Therefore , fatty meal hangs around in stomach for longer time to allow more time for intestinal digestion & absorption

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29
Q

Release of Cholecystokinin (CCK) is stimulated by

A

Fatty acids and monoglycerides in duodenum

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30
Q

Nature’s antacid

A

Secretin

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31
Q

Actions of secretin are?

A

Stimulates pancreatic HCO3 , this in turn neutralizes H+ in the intestinal lumen

Stimulates HCO3 and H2O secretion by the liver, and increases bile production

Inhibit H+ secretion by gastric parietal cells

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32
Q

Secretin is released by

A

S cells of duodenum

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33
Q

Release of secretin is stimulated by?

A

H+ in the lumen of the duodenum

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34
Q

the principle stimulus for delivery of pancreatic enzymes and bile into small intestine

A

CCK

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35
Q

Name 2 Neurocrine “neurotransmitters” Synthesized in neurons in GIT, diffuse across the synaptic cleft to target cell (+ or - )

A

VIP

Enkephalins

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36
Q

Vasoactive intestinal peptide

A

Is released from neurons in mucosa and smooth muscle of GIT

Produces relaxation of GI muscle, including LES

Stimulates pancreatic HCO3 and inhibit gastric H+ (like secretin)

Is secreted by pancreatic islet cell tumor and is presumed to mediate pancreatic cholera

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37
Q

Enkaphalins

A

Are released from nerves in mucosa and smooth muscle of GIT

Stimulates contraction of GI smooth muscles

Inhibit intestinal secretion and fluid and electrolytes.

Therefore, opiates are used in the treatment of diarrhea

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38
Q

This GI neurotransmitter is presumed to mediate pancreatic cholera

A

VIP (Vasoactive intestinal peptide)

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39
Q

This GI neurotransmitter is Produces relaxation of GI muscle, including LES

A

VIP (Vasoactive intestinal peptide)

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40
Q

1/3 of the upper GIT is made of?

A

Striated muscles

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41
Q

Lower 2/3 of upper GIT is made of?

A

smooth muscles

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42
Q

High LES pressure during swallowing

A

Achalasia

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43
Q

Low LES pressure during swallowing

A

GERD

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44
Q

Segmentation contractions

A

In small intestine

mixes the chyme

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45
Q

Peristaltic contractions

A

Moves the chyme in caudal direction

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46
Q

GI smooth muscles are contractile tissues except

A

upper 1/3 of esophagus and external anal sphincter

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47
Q

Circular muscle contraction

A

Decrease diameter

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48
Q

Longitudinal muscle contraction

A

Decrease length

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49
Q

Phasic contractions are

A

periodic contraction and relaxation

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50
Q

Tonic contractions occur in

A

LES and ext. and internal anal sphincter

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51
Q

GI motility is Lowest in ________ and highest in_________

A

the stomach

duodenum

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52
Q

Swallowing is coordinated in?

A

the medulla

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53
Q

Nerves involved in swallowing are?

A

Vagus and glossopharyngeal nerve

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54
Q

Describe the swallowing process

A

Nasopharynx closes, breathing is inhibited

Laryngeal muscles contract and close the glottis

UES relaxes and peristalsis propels food down to stomach

Intra-esophageal pressure = intrathoracic pressure

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55
Q

This drug increases gastric Motility

A

Neostigmine

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56
Q

These drugs decrease gastric tone and motility

A

atropine, meperidine and epinephrine

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57
Q

Gastric contraction increases by ____________ stimulation and decreases by _____________ stimulation

A

vagal stimulation

sympathetic stimulation

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58
Q

Receiving area in gastric motility

A

Fundus and proximal body relax to accommodate meal

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59
Q

Contraction of this area mixes the food and propels it into the duodenum

A

Caudad stomach

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60
Q

Small intestine motility is coordinated by

A

enteric NS

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61
Q

Small intestine is how long

A

4 meter

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62
Q

Characteristics of Small intestine motility

A

4 m long tube

Parasympathetic NS stimulate and sympathetic NS decrease it

Mixing of intestinal contents (chyme)

Propulsion of chyme toward large intestine
Is coordinated by the enteric NS

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63
Q

Characteristics of Large intestine motility

A

Water is absorbed in proximal colon, mass movements propel it into the rectum

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64
Q

Defecation happens when

A

External anal sphincter relaxes, smooth muscle of rectum contracts

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65
Q

Gastrocolic reflex

A

Presence of food in stomach increase motility of colon

Increased stretch by food lead to parasympathetic stimulation

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66
Q

Describe IBS

A

Occurs during stress

Constipation due to increased segmentation contraction

Diarrhea due to decreased segmentation contraction

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67
Q

Vomiting is

A

A wave of reverse peristalsis
UES close – retching
UES open – vomiting

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68
Q

Medullary VC stimulated by?

A

Tickling throat

Gastric distension

vestibular stimulation ( motion sickness)

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69
Q

CTZ in fourth ventricle is stimulated by

A

emetics, radiation and vestibular stimulation.

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70
Q

Vomiting will cause which acid base disturbance

A

Metabolic alkalosis

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71
Q

Droperidol is antiemetic by blocking dopamine receptors and may cause extrapyramidal symptoms. Treatment for extrapyramidal symptoms is

A

Benztropine

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72
Q

Extrapyramidal symptoms

A

These symptoms include dystonia (continuous spasms and muscle contractions), akathisia (may manifest as motor restlessness), parkinsonism (characteristic symptoms such as rigidity), bradykinesia (slowness of movement), tremor, and tardive dyskinesia (irregular, jerky movements).

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73
Q

Contraindicated in parkinson disease

A

Droperidol

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74
Q

Antiemetic of choice for parkinson’s

A

Ondansetron

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75
Q

Characteristics of Metoclopramide

A

Increases LES and gastric motility, decreases tone of pyloric sphincter, relax duodenum

No effect on gastric pH

Increases action of Sux by inhibiting plasma AchEsterase

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76
Q

This drug is used in emesis linked to chemotherapy

A

Ondansetron (Zofran)

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77
Q

Ondansetron (Zofran) characteristics

A

Used in emesis linked with chemotherapy

5-HT3 receptor blocker (5-hydroxytryptamine or serotonin)

Drug of choice for Parkinson’s

S/E headache

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78
Q

The absence of the colonic enteric nervous system, results in constriction of the involved segment, marked dilatation and accumulation of intestinal proximal to constriction , and severe constipation.

A

Megacolon (Hirschsprung’s disease)

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79
Q

Disorders of Swallowing(Dysphagia)

A

CVA (stroke) / cranial nerves damage
Aspiration - UES and pharyngeal contractions are not coordinated
Secondary peristalsis is still functional

Muscular diseases - myasthenia gravis, polio, botulism

Anesthesia - aspiration of stomach contents will cause aspiration pneumonitis (Mendelson syndrome)

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80
Q

Mendelson syndrome

A

aspiration of stomach contents leading to aspiration pneumonitis

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81
Q

Features of CVA (stroke) / cranial nerves damage dysphagia

A

Aspiration because UES and pharyngeal contractions are not coordinated.

Secondary peristalsis is still functional.

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82
Q

The orad region of the stomach includes ____________ whereas the caudad region includes the _____________

A

the fundus and the upper body

lower body and the antrum

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83
Q

Parietal cells (body)

A

Found in the stomach body

Are stimulated by Gastrin, Vagal stimulation, Histamine.

Secrete HCL and intrinsic factor

HCl kills bacteria, breaks down food and convert pepsinogen to pepsin

Intrinsic factor aid vitamin B12 absorption

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84
Q

Chief cell (Body)

A

Found in the stomach body

The secrete pepsinogen which breaks down to pepsin

Secretion is by Vagal stimulation

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85
Q

G cells (Antrum)

A

Found in the Antrum of the stomach

They secrete gastrin which is responsible for stimulating HCl secretion

Secretion is stimulated by vagal vis GRP and inhibited by somatostatin and H+ in stomach

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86
Q

Mucous cells (Antrum)

A

Found in the antrum of the stomach

Its a lubricant that protects the surface from H+

Secreted by vagal stimulation

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87
Q

Identify 3 types of Gastric cells responsible for gastric secretions

A 
Parietal cells (body) ; secretes HCl and IF
Chief cells ( body); secretes pepsinogen
G cells (antrum); secretes gastrin
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88
Q

Mechanism of gastric H+ secretion

A

Parietal cells secretes HCl into the lumen and absorb HCO3

In parietal cell; CO2 +H2O –> H+ + HCO3- catalysed by CA

H+ is secreted into the lumen of the stomach , by H+ - K+ pump (H+, K+ -ATPase). Cl- is secreted along with H+; thus the secretion product of parietal cell is HCl

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89
Q

This drug inhibit the H+, K+ - ATPase and blocks H+ secretion

A

Omeprazole

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90
Q

What is Alkaline tide? Where this HCO3 goes?

A

Refers to a condition, normally encountered after eating a meal, where during the production of hydrochloric acid by parietal cells in the stomach, the parietal cells secrete bicarbonate ions across their basolateral membranes and into the blood, causing a temporary increase in pH.

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91
Q

This drug will cause S/E of hypergastrinemia WHY?

A

Omeprazole

Inhibition of HCl secretion will reduce the concentration of H+ ions in the stomach thereby eliminating the inhibition on Gastrin secretion leading to hypergastrinemia.

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92
Q

What are the 4 mechanism of stumulation of gastric H+ secretion

A

Vagal stimulation

Histamine

Gastrin

Histamine potentiation of actions of Ach and gastrin

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93
Q

Describe gastric H+ secretion via Vagal stimulation

A

Directly by vagus nerve (Muscarinic M3)

Indirectly by stimulating G cells which produce gastrin. Gastrin then stimulates H+ secretion. The neurotransmitter is GRP (not Ach)

Atropine inhibit direct pathway only.

Vagotomy eliminates both direct and indirect pathways

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94
Q

Describe gastric H+ secretion via Vagal stimulation

A

Directly by vagus nerve (Muscarinic M3)

Indirectly by stimulating G cells which produce gastrin. Gastrin then stimulates H+ secretion. The neurotransmitter is GRP (not Ach)

Atropine inhibit direct pathway only.

Vagotomy eliminates both direct and indirect pathways

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95
Q

Describe gastric H+ secretion via histamine

A

Is released from mast cells in the gastric mucosa

Stimulates H+ secretion by activating H2 receptors on the parietal cell membrane

Histamine potentiate the actions of Ach and gastrin

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96
Q

Describe gastric H+ secretion via gastrin

A

Is released in response to eating meal (small peptide, distension of the stomach , vagal stimulation)

Stimulates H+ secretion

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97
Q

This drug inhibit H+ secretion by blocking the stimulatory effect of histamine

A

H2 receptors blockers like cimetidine

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98
Q

This drug inhibit direct pathway of vagal stimulation gastric H+ secretion but has no effect in the indirect pathway

A

Atropine

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99
Q

What are the mechanisms of inhibition of Gastric H+ secretion in the stomach

A

Low pH <3 in stomach- inhibit gastrin secretion

Chyme in duodenum- Inhibits H+ secretion both directly and via GIP ( released by fatty acids in the duodenum) and secretin ( released by H+ in the duodenum)

Prostaglandins- inhibit H+ secretion

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100
Q

Name 3 pathophysiologic conditions of gastric HCl

A

Gastric ulcers
Duodenal ulcers
Zollinger-Ellison syndrome

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101
Q

Gastric ulcers

A

If the normal protective barrier (of mucus and HCO3) of the stomach is damaged, the presence of H+ and pepsin may injure gastric mucosa

Helicobacter pylori has high Urease activity and converts urea to NH3 , which damages the gastric mucosa.

H+ secretion is decresed, not increased (as might be assumed)

Gastrin level are increased ( by -ve feedback ) in patients with gastric ulcer because of lower-than-normal H+ secretion.

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102
Q

Duodenal ulcers

A

Are more common than gastric ulcer

H+ secretion is higher than normal and is responsible , along with pepsin , for damaging the duodenal mucosa

Gastrin levels in response to a meal are higher than normal.

Parietal cell mass is increased because of trophic effect of gastrin

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103
Q

Gastrin secreting tumor

A

Gastrinoma - Zollinger-Ellison syndrome

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104
Q

Pathophysiology of Gastrinoma (Zollinger-Ellison syndrome)

A

Non-beta cell tumor of pancreas (80%) or G-cell tumors in duodenum (10-15%)

Continually secretes large amount of gastrin into blood

Markedly high acid secretion leads to ulcers

20% associated with MEN I

H+ secretion continues unabated because the gastrin secreted by pancreatic tumor cells is not subject to -ve feedback inhibition by H+

Constant stimulation of hyperplastic mucosa

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105
Q

Symptoms of Gastrinoma (Zollinger-Ellison syndrome)

A

Secretory diarrhea because gastrin inactivates lots of digestive enzymes leading to malabsorption.

Weight loss.

Steatorrhea (fatty diarrhea) because pancreatic enzymes are inactivated by very high acid.

Very severe ulcers, ulcers with complications, ulcers are located on atypical places !

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106
Q

Diagnosis of Gastrinoma (Zollinger-Ellison syndrome)

A

High fastening gastrin level (normal < 100 picogram/ml)

Secretin stimulation test

CT to see the tumor

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107
Q

Treatment of Gastrinoma (Zollinger-Ellison syndrome)

A

Medical vs. Surgical

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108
Q

Secretin stimulation test

A

low gastrin levels after IV secretin indicate normal test

High gastrin levels after IV secretin indicate ZE syndrome

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109
Q

Steatorhea in ZE syndrome is due to?

A

The low pH inactivates pancreatic lipase and causes bile salts to precipitate. The result is steatorrhea.

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110
Q

Hypokalemia in ZE syndrome is due to?

A

Hypokalemia results from loss of GI secretions in stool.

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111
Q

Bile contains

A

bile salt
phospholipids
bile pigment ( bilirubin)
water (97%)

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112
Q

Describe emulsification

A

It’s an important step in fat digestion

Bile salts; have both hydrophobic and hydrophilic portions. In aqueous solution, bile salts orient themselves around droplets of lipid and keep the lipid droplets dispersed ( emulsification)

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113
Q

Bile solubilize lipids in _______ for absorption

A

micelles

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114
Q

Describe the process of bile formation

A

Primary bile acids (cholic acid and chenodeoxycholic acid) are synthesized from cholesterol by hepatocytes

Intestinal bacteria convert primary bile acids to secondary bile acids

The bile acids are conjugated with glycine or taurine to form bile salts

During interdigestive period, the GB is relaxed, the sphincter of Oddi is closed and the GB fills with bile
Bile is concentrated in GB by water absorption

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115
Q

Contraction of the bladder can be stimulated by?

A

CCK

Ach

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116
Q

CCK is released in response to?

A

peptide and fatty acids in the duodenum

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117
Q

Bile is recirculates to liver through?

A

terminal ileum

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118
Q

What is the cause of prolonged PT after ileal resection

A

After ileal resection , bile salts are not recirculated to the liver, but are excreted in feces. The bile acid pool is thereby depleted and fat absorption is impaired, resulting steatorrhea (fatty diarrhea). This results in malabsorption of fat soluble vitamins ADEK. Lack of vitamin K results in the inability of the liver to make vitamin k dependent factor 1972

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119
Q

Primary bile acids are?

A

cholic acid and chenodeoxycholic acid

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120
Q

Secondary bile acids are?

A

Deoxycholic acid

Lithocholic acid

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121
Q

primary bile salts are converted to secondary bile salts by?

A

Intestinal bacteria

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122
Q

Lactose intolerance

A

Result from the absence of brush border lastase and the inability to hydrolyze lactose into glucose for absorption

Non-absorbed lactose and H2O remain in the lumen and causes osmotic diarrhea

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123
Q

Carbohydrate digestion and absorption

A

Only monosaccharides are absorbed

Digestive enzymes: alpha amylase, maltase, sucrase, lactase

Na+/glucose cotransport- SGLT-1

Fructose by facilitated diffusion

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124
Q

Identify the 4 Pancreatic proteases responsible for protein digestion? What happens to these enzymes after completion of digestion?

A

Trypsin
chymotrypsin
elastase
carboxypeptidases

After digestive job is done, the pancreatic enzymes degraded and reabsorbed

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125
Q

Optimal pH for Pepsin is

A

1-3

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126
Q

Denaturation of pepsin will occur at what pH?

A

> 5

If intestinal pH is >5, as HCO3- is secreted in pancreatic juice then inactivation of pepsin will occur

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127
Q

Endopeptidases and Exopeptidases are responsible for?

A

Protein digestion

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128
Q

Absorption of proteins is via?

A

Na+ cotransport

Absorb as AA ,dipeptides and tripeptides

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129
Q

Lipid digestion in the Stomach

A

In stomach, mixing breaks lipid into droplets to increase surface area for digestion by pancreatic enzymes.

CCK slows gastric emptying. Thus , delivery of lipids from stomach to duodenum is slowed to allow adequate time for digestion and absorption in the intestine.

130
Q

Lipid digestion in the Small intestine

A

Bile acids emulsify lipids , increasing surface area for digestion.

Pancreatic lipase hydrolyze lipid to FA , monoglyceride, cholesterol.

The hydrophobic products of lipid digestion are solubilized in micelles by bile acids for absorption.

In the intestinal cells, the products of lipid digestion are re-estereified to TG, cholesterol and phospholipids and with apoprotein form Chylomicrons

Chylomicrons are big molecules , so they transferred to lymph vessels and added to bloodstream via the thoracic duct

131
Q

Malabsorption of lipids—Steatorrhea may be due to?

A

Pancreatic disease (pancreatitis, cystic fibrosis)

Hypersecretion of gastrin

Bacterial overgrowth

Tropical sprue: low number of intestinal cells

Failure to synthesize apoprotein B , which lead to the inability to form chylomicrons-abetalipoproteinemia

132
Q

This condition will leads to a depletion of bile acid pool because of the bile acids do not recirculate to the liver

A

Ileal resection

133
Q

Steatorrhea due Low number of intestinal cells.

A

Tropical sprue

134
Q

Failure to synthesize apoprotein B, which lead to the inability to form chylomicrons-

A

abetalipoproteinemia

135
Q

This condition will lead to deconjugation of bile acids and their “early” absorption in the upper small intestine thereby depleting them before they reach small intestine to aid in lipid absorption

A

Bacterial overgrowth

136
Q

Presentation of a patient with malabsorption of lipids

A 
Failure to grow in infancy 
Fatty, pale stools 
Frothy stools 
Foul smelling stools 
Protruding abdomen 
Mental retardation/developmental delay 
Dyspraxia, evident by age ten 
Muscle weakness 
Slurred speech 
Scoliosis (curvature of the spine) 
Progressive decreased vision 
Balance and coordination problems 
Retinitis Pigmentosa
137
Q

Big molecules that are transferred to lymph vessels and added to bloodstream via the thoracic duct

A

Chylomicrons

138
Q

Sodium moves into the intestinal cells by

A

Passive diffusion
Na+ - glucose cotransport– most important
Na+ - H+ exchange

139
Q

Absorption of K+

A

Passive diffusion

Secreted in colon

In diarrhea, K+ secretion by the colon is increased because of flow rate leading to Hypokalemia

140
Q

____________ increases Na+ reabsorption and K+ secretion in small intestine and colon (just like kidneys

A

Aldosterone

141
Q

This condition causes diarrhea by stimulating Cl- secretion via cAMP causing opening of Cl- channels. Na+ and H2O follow Cl- into the lumen and lead to secretory diarrhea.

A

Vibrio cholerae (cholera toxin)

Some strains of E.Coli

142
Q

Vitamins absorption

A

Fat soluble vitamins ( A, D, E, K)
Are incorporated into micelles and absorbed along with other lipids

Water soluble vitamins - By Na+ cotransport

Vit B12 is absorbed in terminal ileum and requires IF

Gastrectomy causes loss of parietal cells which are source of IF leading to Pernicious Anemia

143
Q

Ca++ absorption

A

Depend upon active Vit D

Rickets in children and osteomalacia in adults

144
Q

Iron absorption

A

Is absorbed as heme iron (iron bound to Hb) or as free Fe++.

In the intestinal cells heme iron is degraded, free Fe++ binds to apoferritin and is transported into the blood.

Free Fe++ circulates in the blood bound to transferrin.

Iron deficiency is the MCC of anemia.

145
Q

Diseases that result in decreased absorption even when food is well digested are often classified as

A

Sprue

146
Q

Non tropical sprue

A

also called celiac disease

allergic to gluten (wheat, rye)

destroys microvilli and sometimes villi “bald intestine”

147
Q

Tropical sprue

A
  • bacterium (?)

- treated with antibacterial agents

148
Q

What are the 4 indications of splenectomy

A

Trauma

Idiopathic thrombocytopenic purpura ITP

Thrombotic thrombocytopenic purpura TTP

Hypersplenism

149
Q

Post-splenectomy problems

A

Thrombocytosis- no treatment if < 1,000,000

Sepsis

More common in children

Vaccinate for pneumococcus , hemophilus

Prophylactic antibodies in children

150
Q

Hypersplenism

A

Spleen removes one or more cell lines of blood (RBC,WBC, platelets)

Primary hypersplenism is rare

MC due to portal venous hypertension

Other causes- lymphoma, leukemia, lupus, mononucleosis, hemolytic anemia, thalasemia, sarcoidosis, Gaucher’s disease, malaria

Treatment based on underlying cause

151
Q

Most common cause of hypersplenism is?

A

portal venous hypertension

152
Q

Causes of hypersplenism

A 
portal venous hypertension
lymphoma 
leukemia
lupus
mononucleosis
hemolytic anemia
thalasemia
sarcoidosis 
Gaucher’s disease
malaria
153
Q

Thrombotic thrombocytopenic purpura (TTP)

A

Capillary blocked by platelet deposits.

Fever , hemolytic anemia , renal failure, low platelets ( used up in forming clumps in body).

154
Q

Idiopathic thrombocytopenic purpura (ITP)

A

Most frequent hematologic indication for Splenectomy.

Excess platelet removal and destruction by spleen.

Bleeding with minor trauma.

Childhood form- following URI; self-limiting

155
Q

What is the treatment for TTP

A

Plasmapheresis

Steroids

FFP

Aspirin

Splenectomy for refractory patients has some improvement

156
Q

Treatment of ITP

A

Avoid trauma ( sports)
Steroids
Splenectomy

157
Q

Spleen trauma

A

Abdominal /LUQ pain, shoulder pain (due to irritation of diaphragm), hypotension

Dx- peritoneal lavage, CT

158
Q

Treatment of spleen trauma

A

Avoid Splenectomy if possible

Splenorrhaphy (repair) with mesh, sutures

159
Q

Protrusion of portion of stomach to thoracic cavity

A

Hiatus hernia

160
Q

Hiatus hernia

A

Protrusion of portion of stomach to thoracic cavity

Sliding 30%

Severe reflux

Surgical repair

161
Q

Acute Pancreatitis

A

Pancreatic enzymes are activated in pancreas rather than in intestinal lumen.

162
Q

What are the causes of acute pancreatitis

A

Hypercalcemia/Hyperlipidemia

Trauma (iatrogenic- post ERCP)

Drugs e.g. fursemide, sulfa, estrogen, thiazide

Infection

ETOH and gallstones

163
Q

______________ account for > 90% of cases of acute pancreatitis

A

ETOH and gallstones

164
Q

What are the signs and symptoms of acute pancreatitis

A

Severe epigastric pain to back; increases post-prandial

Peritoneal signs, N/V causing dehydration

Grey-Turner sign

Cullen sign

Pulmonary finding- ARDS (due to elastase)

165
Q

superficial edema with bruising in the subcutaneous fatty tissue around the peri-umbilical region.

A

Cullen sign

166
Q

bruising of the flanks, the part of the body between the last rib and the top of the hip. The bruising appears as a blue discoloration.

A

Grey-Turner sign

167
Q

Lab findings in acute pancreatitis

A

Markedly high amylase, lipase, hypocalcemia , hyperglycemia

CT

ERCP

Ranson’s criteria*

168
Q

Extrahepatic complication of acute pancreatitis is?

A

SHOCK due to loss of lots of fluid “ internal burn”
Pleural effusion, ARDS
ARF (third spacing)
DIC

169
Q

Pseudocyst is a complication of acute pancreatitis and which may?

A 
Bleed
Obstruct
Infected
Leak: ascites, pleural effusion
Needs drainage
170
Q

Name 3 complications of acute pancreatitis

A
  1. Big swollen pancreas
  2. Extrahepatic
  3. Pseudocyst which may bleed, obstruct infect or leak causing ascitis and pleural effusions that need drainage
171
Q

Management of acute pancreatitis involves

A

NPO and NG suction- put the pancreas to rest. “deactivate the gland”

IV hydration- massive volume depletion

Pain meds

Remove the stones!!

ERCP

172
Q

Etiology of chronic pancreatitis

A

Mostly due to ETOH, never from gall stones

Pancreatic duct obstruction

Idiopathic

173
Q

What are the signs and symptoms of chronic pancreatitis

A

Pain, Pain, Pain

Steatorrhea

DM

Malabsroption

174
Q

What are the diagnostic tests of chronic pancreatitis

A

X-ray: calcification of pancreas

Sono

ERCP

175
Q

Treatment therapy for chronic pancreatitis (6)

A
  1. No alcohol
  2. Narcotics
  3. Celiac axis block
  4. Medium chain FA
  5. Pancreatic enzyme supplements
  6. Gastric acid secretion suppression
176
Q

What are the anesthetic considerations for chronic pancreatitis

A
  1. Acute abdomen
  2. Rule out diabetes
  3. Electrolyte disorders
  4. Hypocalcemia
  5. Hypomagnesemia
  6. Hypokalemia
  7. Hypochloremia
  8. Blood coag profile
  9. Kidney profile
  10. Pulmonary assessment
  11. CVS assessment
177
Q

Tumor of neuroendocrine cells of GIT (90%), most commonly the Stomach, ileum and appendix.

A

Carcinoid tumor

178
Q

Carcinoid tumors secrete_______ causing carcinoid syndrome

A

Serotonin

Also cause markedly high levels of bradykinin, prostaglandins, kallikrein and histamine

179
Q

Markedly high levels of bradykinin, prostaglandins, kallikrein and histamine in carcinoid tumors will cause

A 
Skin flushing
Watery diarrhea and abdominal pain
Bronchospasm
Valvular lesions
Large swings in BP
SVT
180
Q

High levels of 5-HIAA (5-hydroxyondoleacetic acid) in urine indicates

A

Carcinoid tumor

181
Q

During anesthesia for a patient with carcinoid tumor, avoid____?

A

Hypotension

Catecholamine

Histamine-releasing drugs e.g. morphine, atracurium

182
Q

Treatment for carcinoid tumors includes this drug.

A

octeroids (somatostatin analogue)

183
Q

Ischemia in 2 of 3 mesenteric vessels: Celiac axis, SMA, IMA

A

Abdominal angina

184
Q

Symptoms of Abdominal angina

A

Post-prandial pain
Sitophobia
Weight loss

185
Q

Diagnostic tests of abdominal angina

A

H&P

Angiogram

186
Q

Treatment of abdominal angina

A

Revascularization

187
Q

Ischemia of SMA

A

Mesenteric Ischemia

188
Q

Mesenteric Ischemia is usually due to?

A

Usually non-occlusive- low flow (CHF, hypotention) vs. occlusive (embolus in A.fib; thrombus)

189
Q

Severe abdominal pain out of proportion to physical finding

A

Mesenteric Ischemia

190
Q

Lab/ diagnostic findings in Ischemia of the SMA

A

High K+

Lactic acidosis

Leukocytosis

“Thumbprinting” on barium enema

Mesenteric angiography

191
Q

This condition predisposes to a risk of intestinal gangrene

A

Mesenteric Ischemia

192
Q

Ischemia of IMA

A

Ischemic Colitis

193
Q

Ischemic Colitis is usually due to?

A

Usually non-occlusive- low flow (CHF, hypotention) and with small vessel disease (therefore angiogram not helpful)

Can occur after AAA repair and IMA damage

194
Q

What are the sigs and symptoms of ischemic colitis

A

Painless bleeding

Typical colitis- bloody diarrhea, pain

Acute left sided abdominal finding

Most commonly in “watershed” areas- splenic flexure and rectosigmoid

195
Q

Treatment of pseudomembranous colitis

A

D/C offending antibiotics
Metronidazole
Oral vancomycin

196
Q

Antibiotic associated colitis

Overgrowth of C. diff

A

Pseudomembranous Colitis

197
Q

Signs and symptoms of Pseudomembranous Colitis

A

Watery diarrhea

Abdominal cramp

Toxic megacolon

198
Q

Pathophysiology of Pseudomembranous colitis.

A

Yellowish plaque-like lesions in colon. Caused by an exotoxin produced by Clostridium difficile that inhibits a signal transduction protein, leading to death of enterocytes.

199
Q

Daily bile production =

A

1200ml

200
Q

Bile vomitus is ____________ while gastric vomitus is ______

A

alkaline

acidic

201
Q

Liver acts as a blood reservoir holding _____ ml

A

500 ml

(Increased liver size in CHF). Sympathetic stimulation results expulsion of blood from liver

202
Q

When BG is high, _________ occurs, when BG is low ,_________ occurs and glucose is released into the blood from the liver

A

glycogenesis

glycogenolysis

203
Q

Functions of the liver

A

Converts non-carbohydrates to glucose.
Oxidizes fatty acids to produce ATP.
Synthesizes lipoproteins, phospholipids, and cholesterol.
Converts carbohydrates and proteins into fats.
Formation of all clotting factors except III & vWF (and IV ‘Calcium’).
Deaminates amino acids.
Synthesizes plasma proteins and amino acids.
Converts some amino acids to other amino acids.
Stores glycogen, vitamins A, D, B12 and iron.
Phagocytosis of worn out RBCs and foreign substances. Kupffer cells (tissue macrophage) are blood cleaner – kill 99% bacteria from gut.
Can regenerates itself
Produces urea in order to remove NH3 (from hepatic deamination process and from bacterial production in the gut)*
Insulin clearance
Detoxification of drugs , poisons, hormones

204
Q

Detoxification of drugs , poisons, hormones by the liver

A

Toxic substances are presented to liver via portal circulation
Liver modifies these substances by “first pass metabolism”
Phase I reactions are catalyzed by cytochrome P-450 enzymes. Important in metabolism of anesthetics These are followed by Phase II reactions that conjugate the substances. Once conjugated the substance can be easily excreted
Tolerance develops due to induction of P-450 by various drugs
Phase II reactions slow down in old age.

205
Q

___________ reactions slow down in old age.

A

Phase II

206
Q

REVIEW IMAGES IN SLIDES 52-62 SECOND PPT. Memorize slide 75

A

REVIEW IMAGES IN SLIDES 52-62 SECOND PPT

207
Q

Site of Portal-systemic Anastomosis

A

Esophagus - esophageal varices
Umbilicus -caput medusae
Rectum - internal hemorrhoids

208
Q

Portal-systemic Anastomosis

A

Varices of gut, butt and caput (medusae) are commonly seen in portal hypertension (high back up pressure)

May cause life-threatening bleeding

Portocaval shunt (connecting portal vein and IVC) is inserted to relieve portal hypertension

209
Q

25-30 % of cardiac output

A

Blood Supply of Liver

210
Q

Liver receive blood from

A

hepatic artery (25%) and from hepatic portal vein (75%)

Oxygen supply is 50:50

211
Q

Normal portal vein pressure =

A

9 mmHg

212
Q

Cirrhosis has high resistance to blood flow, therefore low _________.

A

portal blood flow

213
Q

Liver blood circulation pathway

A

Blood enters via hepatic artery (25%) and hepatic portal vein (75%)

In liver, hepatic artery and portal vein divide and subdivide finally into interlobular vessels.

Interlobular vessels open into hepatic sinusoids.

Thus, hepatic arterial blood mixes with portal venous blood in the sinusoids and flow between hepatocytes.

Hepatic sinusoids drain into interlobular veins which join to form central vein -> hepatic vein -> IVC ->systemic circulation

214
Q

Hepatic blood flow depends on

A

Driving pressure (MAP- hepatic venous pressure)

Intrahepatic vascular resistance

Metabolic demand

215
Q

All volatile anesthetics _______ hepatic blood flow

A

decrease

216
Q

bilirubin is conjugated with glucuronic acid in the liver by?

A

enzyme UDP glucuronyl transferase.

217
Q

LFT: Bilirubin

A

N= 0.5 mg/dl. Elevated in obstructive & hemolytic jaundice

218
Q

LFT: Alkaline phosphatase

A

Raises with biliary tract obstruction , hepatocellular damage

Elevated in osteoblastic bone activity

219
Q

LFT: Gama-Glutamyl transpeptidase (GGT)

A

GGT levels are parallel those of Alk phos

220
Q

LFT: SGOT , SGPT (AST,ALT)

A

Elevated in hepatocellular injury due to leakage ( hepatitis, ischemia)

SGOT in heart , muscle and kidney

221
Q

LFT: GST (Glutathione S-transferase)

A

More sensitive marker of hepatocellular damage

222
Q

LFT: 5ˈ nucleotidase activity

A

Most sensitive marker of hepatocellular damage

223
Q

LFT: LDH

A

High in hepatocellular damage

224
Q

LFT: Albumin

A

Hepatic injury causes low production

225
Q

This LFT raises with biliary tract obstruction

A

Alkaline phosphatase

226
Q

Best indicator of hepatocellular dysfunction ( not making Prothrombin)

A

PT prolongation

227
Q

Last liver function to fail

A

Ammonia conversion to urea

Glucose production ( hypoglycemia is sign of worst prognosis)

228
Q

What are the effects of anesthesia to hepatic function

A

Decreased Blood flow and Drug metabolism

Increased Biliary pressure

Postoperative jaundice- Resorption of large hematoma or hemolysis after transfusion

229
Q

Causes of Hyperbilirubinemia

A

Massive hemolysis with rapid release of bilirubin.

Decrease excretion (e.g. liver damage or bile duct obstruction).

230
Q

Normal level of free bilirubin=

A

0.5 mg/dl

231
Q

bilirubin > 1.5 mg/dl

A

jaundice

232
Q

Van den Bergh test

A

Differentiates between hemolytic jaundice and obstructive jaundice

233
Q

High unconjugated (free) bilirubin in blood

A

hemolytic jaundice

Liver has no time to conjugate due to excessive production of bilirubin in spleen.

234
Q

High conjugated bilirubin in blood

A

Obstructive jaundice

Obstruction is past hepatocytes therefore more conjugated bilirubin

235
Q

In Obstructive jaundice, obstruction may be due to?

A

Gall stones

Cancer of head of pancreas

Damage of hepatic cells e.g. in hepatitis

236
Q

-ve urobilinogen in urine and no stercobilin in stool “ clay color stool” indicate?

A

total obstruction of bile flow

237
Q

high conjugated bilirubin in urine indicates

A

severe biliary obstruction

238
Q

Sign and symptoms of viral hepatitis

A
  1. Dark urine
  2. Fatigue
  3. Anorexia
  4. Fever
  5. Emesis
  6. Headache
  7. Abdominal discomfort
  8. Light-colored stool
  9. Pruritus
  10. Jaundice
  11. Tender hepatomegaly
239
Q

Hepatitis A Virus (HAV)

A

Fecal-oral route, water born, shellfish, gays , IV drug abuser

Short incubation period (3 wk)

Course: cholestatic (high bilirubin) or hepatocellular (high transaminase)

No carriers, not chronic (doesn’t hurt but taste bad!)

Dx: HAV IgM

Exposure: immunize human Ig

240
Q

Hepatitis B Virus (HBV)

A

DNA virus

Parenteral , skin poppers, vertical (mother to neonate) and sexual (50%)

Long incubation period (3 mo)

HBsAg + , HBcAb +

Carriers , lead to chronic

Predispose to cancer

Exposure: vaccine+HBIG

Dx: HBsAg; HBcAb- IgM; HBeAg

241
Q

Hepatitis B Virus (HBV)

A

DNA virus

Parenteral , skin poppers, vertical (mother to neonate) and sexual (50%)

Long incubation period (3 mo)

HBsAg + , HBcAb +

Carriers , lead to chronic

Predispose to cancer

Exposure: vaccine+HBIG

Dx: HBsAg; HBcAb- IgM; HBeAg

242
Q

Hepatitis C Virus (HCV)

A

Skin poppers (60%)

Sexual

Before 90’s – blood transfusion

Carriers

Predispose to cancer, cirrhosis and chronic hepatitis

243
Q

HDVs

A

Defective virus

Requires co-infection with HBV

More severe course- fulminant hepatitis

More prevalent in IV drug abuser, hemophiliacs

244
Q

IgM antibody to HAV; best test to detect active hepatitis A

A

IgM HAVAb

245
Q

HBsAg

A

Antigen found on surface of HBV, indicates active state; Appears before the symptoms, persists 3-4 months , disappears when virus clear. If persistent for > 6 months- carrier state

246
Q

Antibody to ABsAg, appears a few weeks after the disappearance of the antigen and indicates recovery and vaccination (immunity)

A

HBsAb

247
Q

Antigen associated with core of HBV

A

HBcAg

248
Q

Antibody to HBcAg; Only marker during window period. Appears 4 weeks after the appearance of HBsAg, is present during acute illness and can remain elevated for years

A

HBcAb

249
Q

HBeAg

A

A second different antigenic determinant in the HBV core. Important indicator of infectivity ( transmissibility) BEware!

250
Q

Antibody to ‘e’ antigen; indicates low transmissibility

A

HBeAb

251
Q

These drugs can cause acute hepatitis

A

INH

Methyldopa

252
Q

These drugs can cause Cholestasis

A

Chlorpromazine
Erythromycin
Estrogen

253
Q

These drugs can cause Fatty liver

A

Steroids, alcohol (MCC), tetracycline

254
Q

Acetaminophen overdose

A

Dose related

Reduced glutathione stores

Can be severe , fatal

Sky high transaminases- in thousands !

Severe toxicity with low dose = ETOH

Treatment :N-Acetylcysteine

255
Q

Rare, often fatal childhood hepatoencephalopathy

A

Reye’s syndrome

256
Q

Reye’s syndrome Findings

A

Fatty liver

Hypoglycemia “ominous sign”

Coma

Associated with viral infection (VZV, influenza B) and salicylates; thus aspirin is no longer recommended for children (use acetaminophen with caution!)

257
Q

Why should babies not receive baby aspirin.

A

It is associated with reye’s syndrome.

258
Q

Chronic alcoholism is characterized by

A

Thrombocytopenia

Leukopenia

Megaloblastic anemia- Due to dietary deficiency of folate (and thiamine).

MAC elevated in sober and decreased in intoxicated patients.

Bleeding due to sick liver

259
Q

Bleeding due to sick liver can be treated by

A

Platelet transfusion
Vit K
FFP
Cryo

260
Q

Delirim Tremens -DTs

A

Alcohol withdrawal syndrome

After 24-96 hrs cessation of drinking

Restlessness, confusion, agitation and hallucinations

Treatment: Long acting benzo, Antipsychotic

261
Q

ALCOHOLIC HEPATITIS

A

Most common drug induced hepatitis

Low portal blood flow (due to high resistance).

Oxygen delivery depends on hepatic artery blood flow

Avoid hypotension during anesthesia

Clinical : fever, tachycardia, jaundice , RUQ symptoms

Lab: SGOT (AST) to SGPT (ALT) ratio is greater than 1.5 (AST>ALT)

262
Q

SGOT (AST) to SGPT (ALT) >1.5

A

ALCOHOLIC HEPATITIS

263
Q

General characteristics of fatty liver

A

Disease of fat people, reversed by weight loss

Common cause of asymptomatic LFT abnormalities

Microvesicular fat vs. macrovesicular fat

264
Q

Chronic Hep B

A

Persistence of LFT’s abnormalities > 6 months

Sx: asymptomatic carrier vs chronic active disease

Prognosis: cirrhosis and hepatoma

Tx: alpha-interferon

265
Q

Chronic Hepatitis C

A

Frequent progression to chronic hepatitis and cancer (20X)

Tx: alpha-interferon

266
Q

Chronic Autoimmune hepatitis

A

Typically disease of women

May be hirsute, Cushinoid

Dx: Anti smooth muscle antibody

Tx: immune suppression : steroid

267
Q

Anesthetic consideration in Hepatitis

A

Less anesthetic is needed

Aspiration precaution must be implemented

Increase risk of surgical bleeding

Brain less tolerant to hypoxia

Decrease neurotransmitter uptake => increase levels of catecholamine

268
Q

Copper overload creating copper accumulation in liver, brain, cornea

A

Wilson’s disease

269
Q

Elevated ceruloplasmin; Low serum copper

A

Wilson’s disease

270
Q

Keyser-Fleischer ring at rim of cornea

A

Wilson’s disease

271
Q

D-penicillamine

A

treatment for wilson’s disease

272
Q

Features of Wilson’s disease

A

Copper overload creating copper accumulation in liver, brain, cornea

Elevated ceruloplasmin; Low serum copper

Asymptomatic

Chronic active hepatitis , fulminant hepatic failure

Neuropsychiatric; dementia

RTA

Keyser-Fleischer ring at rim of
cornea

273
Q

Hemochromatosis

A

Hyper-absorption and deposition of iron in many organs

Secondary to multiple blood transfusion

Elevated ferritin and % Fe sat

274
Q

Hyper-absorption and deposition of iron in many organs

A

Hemochromatosis

275
Q

Clinical features of Hemochromatosis

A

Liver diseases => cirrhosis => hepatoma

DM ( ‘Bronze’ diabetes)

Arthropathy

Cardiomyopathy

Impotence ( due to pituitary dysfunction “hypo pit”)

276
Q

Treatment of hemochromatosis

A

Repeated phlebotomy, deferoxamine

277
Q

This patient has enough in the body to set off metal detectors

A

hemochromatosis

Iron~50 g

278
Q

alpha 1-Antitrypsin deficiency

A

Autosomal recessive

High trypsin level; a proteolytic substance

Rare syndrome of progressive cirrhosis

With or without pulmonary disease

279
Q

alpha 1-Antitrypsin deficiency

A

Autosomal recessive

High trypsin level; a proteolytic substance

Rare syndrome of progressive cirrhosis

With or without pulmonary disease

280
Q

Findings of alpha 1-Antitrypsin deficiency

A

Emphysema

Neonatal hepatitis; chronic hepatitis in adults

Cirrhosis and hepatoma

281
Q

Low alpha-1 antitrypsin level is diagnostic for?

A

alpha 1-Antitrypsin deficiency

282
Q

Treatment for alpha 1-Antitrypsin deficiency

A

Treatment of complication
Hepatoma surveillance
Liver transplant for end-stage liver disease

283
Q

Diffuse fibrosis of liver that destroys normal architecture. Widespread nodule formation in the liver.

A

Liver cirrhosis

284
Q

Distortion of liver anatomy in Liver cirrhosis

causes?

A

Decreased blood flow leading to portal hypertension and back streaming.

Liver failure.

285
Q

Causes of Liver cirrhosis (9)

A 
Ethyl alcohol EOH (MCC)
HBV
HCV
PBC (Primary biliary cirrhosis) 
CHF
Autoimmune
hemochromatosis
Wilson’s disease
Alpha 1 antitrypsin deficiency
286
Q

Differentiate between micronodular and macronodular in liver Cirrhosis

A

Micronodular: nodules < 3 mm, uniform size. Due to metabolic insult (e.g. alcohol)

Macronodular: nodules > 3 mm, varied size. Due to significant liver injury, leading to hepatic necrosis (e.g. post-infectious or drug induced hepatitis). Increased risk of hepatocellular Ca.

287
Q

Effects of portal hypertension (low BF through liver)

A

Bleeding from esophageal and gastric varices => hematemesis, melena

Splenomegaly, cardiomyopathy
Caput medusae (distension of abdominal wall veins)

L albumin => ascites => decrease FRC
Due to excessive hydrostatic pressure liver “sweating” occurs. Also due to low albumin
Abdominal distention, shifting dullness (+ve)

Testicular atrophy

Hemorrhoids, esophageal varices “back stream”

288
Q

Effects of liver cell failure

A

Bleeding tendency (Low prothrombin). Major cause of morbidity and mortality.

Hepatic encephalopathy (due to High NH3)

Scleral icterus

Fetor hepaticus (bad breath like corpse)

Spider navi

Gynecomastia, Loss of sexual hair (due to decreased breakdown of estrogen)

Jaundice

Liver “flap” : coarse hand tremor

Anemia ,low PO2

Impair protein synthesis => increase third spacing => Increase effect of protein bound drugs e.g. barbiturates

Hepatic encephalopathy => coma

289
Q

Treatment of cirrhosis

A

Lactulose (lactic acid) converts NH3 to NH4+ that is poorly absorbed and thus excreted (Base+ Acid => ionized form)

Gut sterilization by neomycin enema kills intestinal bacteria responsible for NH3 production

Protein restricted diet

Maintain BP to maintain hepatic artery blood flow

290
Q

BP should be maintained in liver cirrhosis to maintain hepatic artery blood flow because

A

Oxygen supply largely depends on hepatic artery blood flow as portal blood flow decreased in cirrhosis.

Remember portal vein supplies 50% 02 same as hepatic artery

291
Q

Anesthetic consideration for a patient with liver cirrhosis

A

High dose of non-depolarizing NM blockers is needed (due to increase volume of distribution)

Sux toxicity due to deficient plasma cholinesterase

292
Q

Mnemonic AC, 9H in liver cirrhosis refers to?

A 
Ascites
Coagulopathy
Hypoalbuminemia
Portal Hypertension
Hyperammonnemia
Hepatic encephalopathy
Hepatorenal syndrome
Hypoglycemia
Hyperbilirubinemia/jaundice
Hyperestrinism
Hepatocellular carcinoma
293
Q

High pressure in portal vein ( >10 mmHg)

A

Portal Hypertension

294
Q

Most common cause of portal hypertension is?

A

Alcoholic cirrhosis (Fibrosis in liver, high resistance to portal vein)

295
Q

Patient with portal hypertension is Prone to massive bleeding because?

A

Backward pressure => congestive splenomegaly => platelet sequestration => thrombocytopenia

Impaired coag factor production

296
Q

drugs for treatment for portal hypertension

A

Propranolol

Vasopressin +NTG

297
Q

Treatment of portal hypertension

A

Endoscopic sclerotherapy

Banding

Portocaval shunt

298
Q

Encephalopathy is an Adverse effect of portocaval shunt because?

A

Blood is bypassing the liver, no detoxification.

299
Q

Portal hypertension Risk factor bleeding

A

variceal size

endoscopic stigmata

300
Q

Preoperative Anesthetic considerations for a patient with portal hypertension

A

Wait till normalization of LFTs

LFT, Lytes, HBsAg

High PT => Give Vit K and FFP

301
Q

Intraoperative Anesthetic considerations for a patient with portal hypertension

A

Inhalation A. are preferable to IV A. => Isoflurane is agent of choice for maintaining hepatic blood flow.

Avoid decrease in hepatic blood flow (low O2 delivery) due to: Hypotension; Excessive sympathetic activation; High mean airway pressure.

Regional anesthesia is useful in advanced liver disease

Greater loading dose and smaller maintenance doses of muscle relaxant

302
Q

Gall stones Form when

A

solubilization bile acids and lecithin are overwhelmed by increased cholesterol and/or bilirubin. OR “too much water absorption”

303
Q

Risk factors for gallstones (4 F’s)

A

Female
Fat
Fertile
Forty

304
Q

Gall stones May present with Charcot’s triad which is?

A

Epigastric/RUQ pain radiating to shoulder

Fever

Jaundice

305
Q

Describe Three types of Gall stones

A

Cholesterol stones: MC,associated with obesity, Chron’s disease, C.fibrosis, advanced age, estrogen, multiparity, rapid weight loss and Native American origin

Mixed stones: have both cholesterol and pigment component.

Pigment stones: seen in pt with chronic RBC hemolysis, alcoholic cirrhosis, advanced age, and biliary infection

306
Q

Cholesterol stones are most commonly associated with?

A 
obesity 
Chron’s disease
C.fibrosis
advanced age
estrogen
multiparity
rapid weight loss
Native American origin
307
Q

Diagnosis and treatment of gallstones

A

Dx with sono

Tx with cholecystectomy

308
Q

Physiological jaundice of newborn

A

During 1st week
High unconjugated bilirubin

No clinical importance

Due to deficiency of glucuronyl transferase in the immature liver; in primies

Tx: Phototherapy

309
Q

Prehepatic hepatic dysfunction lab findings and causes

A

Bilirubin: High unconjugated

Aminotransferase: Normal

Alkaline phosphatase: Normal

Causes: Hemolysis, Hematoma resorption, Bilirubin overload from whole blood transfusion

310
Q

Intrahepatic (Hepatocelluar) hepatic dysfunction lab findings and causes

A

Bilirubin: High conjugated

Aminotransferase: Markedly high

Alkaline phosphatase: Normal or slightly high

Causes: Viral, Drugs, Sepsis, Hypoxemia, Cirrhosis

311
Q

Posthepatic (cholestatic) hepatic dysfunction lab findings and causes

A

Bilirubin: High conjugated

Aminotransferase: Normal or slightly high

Alkaline phosphatase: Markedly high

Causes: Stones, Sepsis

312
Q

Most common Congenital Hyperbilirubinemia

A

Gilbert syndrome

313
Q

Congenital Hyperbilirubinemia marked by low uptake of bilirubin by liver cells and decreased activity of glucuronyl transferase

A

Gilbert syndrome

314
Q

Severe form of Congenital Hyperbilirubinemia marked by early death and damage to basal ganglia.

A

Grigler-Najjar syndrome

315
Q

Congenital Hyperbilirubinemia marked by Defective bilirubin transport

A

Dubin-Johnson syndrome

316
Q

Compare the pathophysiology of Primary Biliary Cirrhosis and Primary sclerosing Cholangitis

A

PBC: Autoimmune reaction leading to Destruction of microscopic biliary ductules.

PSC: Idiopathic intra or extra hepatic bile duct fibrosis leading to stricturing that cause obstruction

317
Q

Compare the presentation of Primary Biliary Cirrhosis and Primary sclerosing Cholangitis

A

PBC: Middle-age women, Pruritus (high bile salts) , jaundice, dark urine, light stool, hepatosplenomegaly, Vit ADEK deficiency .

PSC: Pruritus (high bile salts) jaundice, dark urine, light stool, hepatosplenomegaly

318
Q

Compare the labs of Primary Biliary Cirrhosis and Primary sclerosing Cholangitis

A

PBC: High conjugated bilirubin, high Alk P, high cholesterol

PSC: High conjugated bilirubin and Alk P

319
Q

Compare the treatment of Primary Biliary Cirrhosis and Primary sclerosing Cholangitis

A

PBC: Liver transplant

PSC: ERCP

320
Q

Compare the diagnosis of Primary Biliary Cirrhosis and Primary sclerosing Cholangitis

A

PBC: Elevated Anti-mitochondrial antibodies; Liver biopsy to confirm diagnosis

PSC: Associated with ulcerative colitis; US

321
Q

peptic ulcer desease

A

Pain Greater with meals: weight loss

Helicobacter pylori infection in 70%; NSAID (inhibit PG secretion)

Due to low mucosal protection against gastric acid

High in smokers, ETOH, stress ‘type A’ personality

A&P III (6 decks)

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