Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 3 > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Describe Type 1 Diabetes

A
  • Autoimmune destruction of Beta cells
    • No insulin made
  • Insulin injections required or islet transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe Type II diabetes

A
  • Beta cell exhuastion because of hyperglycemia and more insulin is required to produce same effect
  • Decreased insulin (relative to high glucose)
  • hyperglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can occur when blood glucose are chronically too high?

A
  • Blindness
  • Limb amputations
  • Kidney disease
  • Increases risk of heart disease
  • Neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is glucose homeostasis?

A
  • ~5.5 mM and very stable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Function of Glucagon

A
  • Secretion by alpha cells
    • stimulated by low insulin
  • Cause glucose secretion and raises blood sugar
  • Anti-hypoglycemic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Function of Insulin

A
  • Secreted by Beta cells
    • high insulin inhibits alpha cells
  • Causes glucose clearance and removal from blood and stored into tissues
    • no insulin = no glucose clearance = hyperglycemia
  • Anti-hyperglycemic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Function of Somatostatin

A
  • Secreted by Delta cells
  • Regulates both glucagon and insulin levels by preventing their secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How are blood insulin levels measured?

A
  • insulin and C peptide are secreted 1:1
  • C peptide isnt internalized as quickly so it stays in the blood longer and can be measured
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the life threatening acute problems in glucose homeostasis and metabolism that occur in type I diabetes?

A
  • Ketoacidosis - unopposed glucagon because there is no insulin
  • Hypoglycemia - too much insulin injected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How are insulin and glucagon levels altered by both carbohydrate and protein meals?

A
  • [Insulin] changes by a lot (10x)
  • glucagon only changes a little
    • release during a high protein meal is stimulated by arginine

Ratio of insulin: glucagon is more important than the concerations themselves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does insulin affect fat cells?

A
  • insulin effects in adipocytes is much larger than muscle
    • have much fewer GLUT4 transporters on membrane
    • lower basal level and stimulation causes a huge increase when compared to muscle
  • very low levels of insulin will still inhibit lipolysis, so other hormones/stimuli are required to mobilize energy stored in fat during a fast
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the major site of glucose disposal after a meal?

A
  1. Muscle ~50g
  2. Liver ~17g
  3. Brain ~15g
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does insulin affect muscle?

A
  • High insulin increases glucose transport 4x
    • rate limiting but esstential for efficient glucose clearance from blood
    • exercise stimulates GLUT4 receptors to cell surface to increase blood clearance
  • Stimulates glycogen synthesis and inhibits glycogen breakdown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is GLUT1 found and its affinity?

A
  • Pancreatic alpha cells and most other tissues
  • High affinity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where is GLUT2 found and what is its affinity?

A
  • Pancreatic beta cells, liver, intestine
  • low affinity
    • allow glucose to flow down its concentration gradient
  • insulin sensing
    • small changes in [glucose] are amplified due to low affinity of GLUT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where is GLUT3 found and what is it affinity?

A
  • Brain and placenta
  • VERY high affinity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where is GLUT4 found and what is its affinity?

A
  • skeletal muscle, fat, heart
  • high affinity
  • insulin regulated
    • glucose is rate-limited by the total # of GLUT4 transporters which increases with insulin and exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe high affinity GLUTs

A
  • Nearly saturated at basal level
    • no change in glucose uptake under normal glucose fluctations unless total # of GLUTs on surface changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe low affinity GLUTs

A
  • Not saturated at normal blood glucose levels
  • glucose uptake changes over all ranges of [glucose]
    • is how glucose level sensed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What occurs to beta cells secreting insulin during fasting?

A
  • low (basal) glucose _<_5.5 mM
  • ATP/ADP ratio is low
    • ATP sensitive K channel activated (by low ATP)
    • inhibits Ca channel -> causes low (inhibited) insulin secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What occurs to beta cells secreting insulin at the fed state?

A
  • High Glucose levels >5.5mM
  • ATP/ADP ratio increases
    • ATP sensitive K channel inhibited by ATP
    • Activates Ca channel
  • Insulin release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How are alpha cells glucagon secretion altered?

A
  • GLUT1 has high affinity so changes in [glucose] on ATP/ADp are muted
    • receptors are saturated at basal [glucose] cant detect changes in glucose unless # of GLUTs change
  • Insulin regulates glucagon
    • low insulin ->stimulate alpha cells
    • high insulin-> inhibits alpha cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do sulfoylureas do?

A
  • Oral hypoglycemic agent that inhibits Katp channels
  • Causes insulin to be secreted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What do incretins do?

A
  • primes the vesicles to responed to increased Ca2+
  • results in insulin to be secreted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does metformin do?

A
  • Activates AMPK in muscle (mimics exercise)
  • increases insulin sensitivity in muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the roles of cholesterol?

A
  • make membranes more rigid
  • precursor to bile salts/acids
  • Precursors to hormones
    • progesterone
    • estrogens
    • testoterone
    • cortisol
    • aldosterone
  • Precursor to Vit. D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How is cholesterol carried in the blood?

A
  • Cholesterol ester
    • combination of cholesterol and either Fatty Acyl-CoA or Lecithin
  • Concentration in blood 150-240 mg/dl, 2x glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does Acetyl-CoA get into the cell to synthesize cholesterol?

A
  • •Pyruvate > OAA > (add acetyl-CoA) > citrate > citrate transporter crosses inner/outer mito membrane to cytosol > citrate > (dumps acetyl-CoA) > OAA > malate > (gives off NADPH) > pyruvate > crosses membrane back to matrix
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is special about cholesterol synthesis?

A
  • humans synthesize a little less than half of cholesterol we have from Acetyl-CoA rest comes from diet
    • eat more, make less
    • eat less, make more
  • Sources of Acetyl-CoA: FA, carbs ->pyruvate
  • NADPH made in last step will be used for HMG-CoA reductase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the first step of cholesterol biosynthesis?

A
  • Acetoacteyl CoA + Acetyl-CoA -> HMG-CoA
    • enzyme: HMG-CoA synthase
    • requires H2O
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the second step of cholesterol?

A
  • HMG-CoA -> mevalonate
    • enzyme: HMG-CoA reductase
    • Requires: 2 NADPH + 2H+
  • rate limiting step
    • statins work at this step
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the types of regulation of HMG-CoA reductase?

A
  • Feedback inhibtion
    • higher cholesterol, you make less
    • less cholesterol, you make more
  • Phosphorylation/dephosphorylation of HMG-CoA reductase
    • Phosphorylation (AMPK) -> inactive
    • Desphorylation (by HMGRP) -> more active
  • Control of gene expression (Sterol Receptor Element Binding Protein)
    • during normal levels SREBP is anchored in ER membrane. At low sterol levels, SREBP is cleaved and it enters nucleus and increases synthesis of HMG-CoA reductase
  • Rate of enzyme degradation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How do statins work?

A
  • Lipitor and Mevacor are competitive inhibitors of HMG-CoA reductase
  • Side effects
    • can lead to decreased CoQ10 and can lead myopathy and rhabdomyolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Outline the conversion of mevalonate to cholesterol

A
  • C5 to C10 to C15. Two C15s condense to C30 (squalene) to C27 (cholesterol)
  • 19+ steps between squalene to cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the major metabolic fate of cholesterol? How is it used?

A
  • Conversion by liver cytochrom P450 to bile acids
    • stored in gall bladder
    • cholesterol still present in bile acids and can turn to gall stones
  • Transported to small intestine
    • function: solubilize lipids
  • 90% of bile salts are reabsorbed and recycled by colon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How are bile acids made in bile salts?

A
  • CO2- is switched for SO3-
  • Salt conjugates make better solubilizing agents than acids
    • pka of conjugates 1-4
    • pH of duedenum 3-5
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is cholestyramine?

A
  • Not absorbed by the body
    • ionic binding ((-) bile acids bine to (+)-nitrogen on cholestyramine)
  • Removes cholestyramine and cholestrol from the body
    • more cholesterol is converted to bile salts, lowering cholesterol levels
  • Used to be main cholesterol drug before statins but causes gas and diarreha and makes people uncomfortable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Name the different types of pancreas regions and cells

A
  • Exocrine
    • Pancreatic acinar cells
    • centroacinar cells
    • acinar vascular system
  • Endocrine
    • Islets of Langerhans
    • Insuloacinar portal system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe Pancreatic Acinar cells

A
  • produce, store and release digestive enzmes
    • zymogen granules
    • each granule has a different combo of enzymes depending on diet
    • cell makes trypsin inhibitor to protect itself
  • release of enzymes drive by hormones and parasympathetic nerves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe Centroacinar cells

A
  • Modified intercalacted duct cells
  • Located with the acinus
  • Produce bicarbonate - rich buffer
    • adjust acicic chime to optimal pH for pancreatic enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Describe Islets of Langerhans

A
  • scattered among exocrine secretory acini
  • principal cells
    • Alpha, Beta, and Delta cells
  • Minor cells
    • PP cell (F cell)
    • D-1
    • EC cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What do PP Cell (F cell) secrete?

A
  • Pancreatic polypeptide
  • stimulates gastric chief cells
  • inhibits
    • bile secretion
    • intestinal motility
    • pancreatic enzymes
    • HCO3 secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What do D-1 cells secrete?

A
  • Vasoactive intestinal peptide (VIP)
  • simliar to glucagon (hyperflycemia and glycogenolytic)
  • affects secretory activity and mitility in gut
  • stimulates pancreatic exocrine secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What do EC cells secrete in the pancreas?

A
  • Secretin
    • locally stimulates HCO3- secretion
    • stimulates pancreatic enzyme secretion
  • Motilin
    • increases gastric and intestinal motility
  • Substance P
    • NT properties
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How is there duel control of the secretion of pancreatic enzymes?

A
  • peptides secreted by enteroendocrine cells (EC) in duodenum
  • peptide hormones synthesized in endocrin pancreas (islets of langerhans)
  • Stimulate secretion
    • VIP
    • Insulin
    • CCK
  • Inhibit secretion
    • Glucagon
    • PP
    • Somatostatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the insuloacinar portal?

A
  • Each islet is supplied by a network formed by afferent arterioles capillaries lined by fenestrated endothelial cells
  • islets puts all of its hormones in the insulacinar portal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the acinar vascular system?

A
  • independent arterial system that supplies pancreatic acini
48
Q

What are the major functions of the liver?

A
  • Produce most circulating plasma proteins
    • albumin
    • lipoproteins
    • glycoproteins
  • store and convert several vitaminas and iron
  • involved in many metabolic pathways
  • degrades drugs and toxins
  • bile production (exocrine)
  • ability to modify structure of many hormones (endocrine)
49
Q

What is the protal area?

A
  • Hepatocytes are arranged in a hexagon shape, where three classic lobules join together
  • Portal area in the middle
    • Hepatic artery
    • portal vein
    • Interlobular bile duct
    • lymphatic vessels
50
Q

What is the liver acinus (Acinus of Rappaport)?

A
  • concept module of the hepatocytes arrangement based on blood flow
  • 3 poorly defind surrunding a distributing artery in center
  • Zone 1-3
  • Provides best correlation between blood perfusion, metabolic and liver patholgy
51
Q

Describe zone 3 in a hepatocyte

A
  • Closest to central vein
  • most oxygen poor zone
  • first to show ischemic necrosis
  • first to show fat accumulation
  • Key glycolysis enzymes
  • key FA-synthesizing enzymes
52
Q

Describe zone 1 in a hepatocyte

A
  • Closest to portal triad
  • richest in oxygen, nutrients, and toxins
    • key glucose liberating enzymes
    • key FA oxidation enzymes
  • firs to show signs of morphological chnages after bile duct occlusion
  • in ischemia - last to die/first to regenerate
53
Q

Describe the cellular contents of a hepatocyte

A
  • lots of free ribosomes, rER and Golgi apparatus
    • some golgi near bile canaciculi
  • 2k mito
  • many endosomes, lysosomes, peroxisomes
  • Smooth ER
  • two domains
    • lateral (apical)
    • siusodial (basolateral)
54
Q

What is the function of smooth ER in hepatocytes?

A
  • important in detoxification
  • enzymes necessary for detox are in the sER membrane
  • sER highest in zone 3
    • increases if more toxins present
    • detox inactivated by methylation, conjugation, or oxidation
    • detox can happen in peroisomes
55
Q

Describe the lateral (apical) zone of the hepatocyte

A
  • covered with microvilli
  • separated by elaborate intercellular spaces that form bile canaliculi that will eventually flow out of
56
Q

Describe the sinusodial (basolateral) domain of hepatocytes

A
  • microvilli project into space of Disse
    • increase surface area by a factor of 6
    • facilitate exchange of material between hepatocyte and space of Disse
57
Q

What are the two cell types that line the hepatic sinusoids?

A
  • discontinuous endothelial cells
  • Kupffer’s cells
58
Q

Describe the purpose of hepatic sinusoids

A
  • lie between hepatic plates
  • empty directly into central veins
  • hepatic portal veins and hepatic artery empties directly into sinusoids
59
Q

What are Kupffer cells?

A
  • differentiated phagocytic cell derived from monocytes
  • in hepatic sinusoids
  • phagocytosize blood-borne foreign paticulate matter and worn out RBCs
60
Q

Describe the space of Disse

A
  • site of exchange of materials and blood plasma between blood and hepatocytes
  • hepatocyte microvilli absorb nutrients, oxygen, toxins adn release thier metabolic products and endocrine secretions
  • serves as liver’s lymphatic system (lymphatic drainage opposite of blood flow)
  • hepatic stallate cells
61
Q

What are hepatic stallate cells (cells of Ito)?

A
  • Store Vitamin A
  • in pathological conditions differentiate into myofibroblasts adn synthesize collagen, leading to liver fibrosis
62
Q

What is the function of the gall bladder?

A
  • concentration and store of bile between meals
  • release bile by contraction of muscularis in response to CCK from duodenum EC cells
  • regulation of hydrostatic pressure within biliary tract
63
Q

Describe the mucosa of gall bladder

A
  • simple columnar epithelium
    • apical microvilli
  • concentration of bile requires couped transport of salt and water
    • Na pump on lateral surface to facilitate h20 absorption from bile
  • typical lamina propria
64
Q

Describe the muscularis layer of gall bladder

A

there is NO muscularis mucosae or submucosa muscularis in the gall bladder

  • Interwoven SM to contract complete
  • contraction trigged by dietary fat in duodenum and EC cells secrete CCK
65
Q

Describe outer layer of the gall bladder

A
  • Adventitia attaches gall bladder to liver
  • Serosa covers its free peritoneal surface
66
Q

What is the gastro-esophageal junction just below the diaphragm?

A

cardiac orifice

  • this is where the stomach begins
67
Q

What are the divisions of the stomach and what seperates them?

A
  • Fundus
    • stomach aboce the cardiac orifice
  • Body
    • from cardiac orifice to Veing of Mayo
  • Antrum
    • from angular incisure (notch/indentation on lesser curve) to pyloric canal
    • where vein of mayo crosses stomach
  • Pylorus
    • canal and sphincter
68
Q

How is a peptic ulcer disease treated?

A
  • peptic ulcer more common in duodenum
  • surgical removal of acid forming portion of stomach (antrectomy) and a vagotomy (cutting the vagus nerves)
69
Q

How is pyloric stenosis treated?

A
  • seen in infants and have hypertrophy of pyloric muscle that causes gastric obstruction
  • treatment is pyloromytomy - cutting of muscle to open pyloric canal
70
Q

What is the arterial supply of stomach?

A
  • All three branches of celiac axis
    • Common hepatic artery
      • right gastric artery off the proper hepatic artery
        • antrum and pylorus
      • right gasro omental artery off the gastroduodenal artery
        • greater curvature from antrum to mid body
    • Splenic Artery
      • short gastric arteries
        • greater curvature from fundus to upper body
      • Left gastro-omental artery
        • anastomoses with R gastro-omental
        • greater curvature from fundus to upper body
    • Left Gastric Artery - supplies upper stomach and lower esophagus
71
Q

What is the venous drainage of stomach?

A
  • Parallels arterial supply of stomach
  • veins coalesce and drain into portal vein
    • r/l gastric veins -> portal vein
    • R gastro-omental vein ->SMV
    • L gastro-omental vein -> splenic vein
72
Q

Where is there lympathic drainage of stomach?

A
  • Left gastric lymph nodes
  • Gastro-omental lymph nodes
  • Pyloric lymph nodes
  • pancreaticolienal lymph nodes
  • R gastric lymph nodes

All lymph nodes drain into celiac axis lymph nodes

73
Q

What is the cisterna chyle?

A
  • celiac lymph nodes drain itno cisterna chyle
  • Cisterna chyle is a dilation of convergence of lymphatic channels and drains into thoracic duct
  • right crus of the diaphragm
74
Q

How does the vagus nerve innervate the stomach?

A
  • Procides motor nerves to stomach and stimulation for acid production
  • Left vagus nerve
    • anterior vagus trunk - enters along lesser curvature and banches to anterior stomach, liver, and duodenum
  • Right vagus nerve
    • posterior vagus truck - enters lesser curvature and branches to posterior stomach
75
Q

What are the borders of the duodenum?

A
  • After pylorus of stomach
  • Ends at ligament of Trietz
76
Q

What are the portions of the duodenum?

A
  • All portions except for first one is complete retroperitoneal
  • First portion
    • duodenal bulb
    • common bile duct, gastroduodenal artery and IVC run posterior to it
  • Second portioin
    • C loop
    • where the pancreatic and common bile duct drain into duodenum through ampulla of vater
  • Third portion
    • horizontal portion
    • where duodenum goes over spine from right to left and ends at SMA
  • Fourth portion
    • begins left of SMA
    • Ends at ligament of Trietz
    • ascending portioin
77
Q

What is the blood supply to duodenum?

A
  • superior pancreticoduodenal artery from gastroduodenal artery
  • Inferior pancreaticodudenal artery from SMA

Drainage

  • Superior mesenteric vein entering portal system
78
Q

What is malrotation?

A
  • the small intestine does not return in a rotated position
  • present with bilious vomiting
79
Q

What are some external features of the jejunum?

A
  • usually thicker and more muscular
    • circular folds (plicae circulares) in mucous membrane are large and well developed
    • more absorptive surface
  • more proximal portion and resides in upper abdomen
80
Q

What is the blood supply to the small intestine?

A
  • entire blood supply from SMA
  • 15-18 branches to jejunum and ileum with collateral circulation through various branches
81
Q

What is the lymphatic drainage in the small intestine?

A
  • lacteals are lyphatics in intestinal villi
    • drain into lymph vessel plexus in mesentery
    • plexus drains into mesenteric lymph nodes
      • Next to intestine
      • along arterial arcades
      • along SMA
  • lymphatics will drain into cisterna chyli and into thoracic duct
82
Q

What is the innervation of the small intestine?

A
  • parasympathetic from vagus - stimulates motility
  • sympathtic from superior mesenteric ganglion
    • T9 and T10
    • pain comes through thoracic segments
83
Q

What is teniae coli?

A

three longitudinal muscle bands that run along the entire colon

84
Q

What is haustra coli?

A
  • permanent sacculations between teniae involving circular muscle but go away in the rectum
85
Q

What are the fatty appendages attached to teniae?

A

appendices epiplociae

86
Q

Describe the cecum

A
  • begins at ileocecal valve
  • sac like structure
  • blood supply
    • ileocolic artery - branch of SMA
87
Q

Describe Vermiform appendix

A
  • function unknown
  • at base of cecum
  • blood supply - ileocolic artery
  • Appendicitis
    • periumbilical pain moving to r lower quadrant
    • nausea +/- vomiting
    • fever is a later finding
88
Q

Name the portions of large intestine

A
  • Ascending or right colon
    • retroperitoneal, right colic artery
  • Transverse colon
    • intraperitoneal, middle colic artery
  • Descending or left colon
    • retroperitoneal, left colic artery
  • Sigmoid colon
    • intraperitoneal, sigmoid arteries
  • Rectum
    • retroperitoneal, superior rectal artery, middle and inferior rectal arteries
89
Q

What are the structural features of the rectum?

A
  • internal folds
    • continuations of teniae
    • supports feces
  • since rectum goes through pelvic floor, there are no diverticuli
90
Q

What is the lymphatic drainage of larges intestine?

A
  • Cecum/appendix
    • periappendiceal LN -> Superior mesenteric Ln
  • Ascending colon
    • paracolic LN -> Superior mesenteric LN
  • Transverse
    • Superior mesenteric LN
  • Descending colon
    • inferior mesenteric LN
  • Sigmoid colon
    • inferior mesenteric LN
  • Rectum
    • Pararectal LN -> inferior mesenteric LN
    • Internal iliac LN
91
Q

What is the innervation of large intestine?

A
  • Colon by Superior mesenteric plexus and inferior mesenteric plexus
  • Rectum by middle rectal plexus from inferior hypogastric plexus
92
Q

Describe the anus

A
  • Begins at puborectalis muscle
  • internal (involuntary) and external (voluntary) anal sphincter
    • external innervated by inferior rectal nerve
  • superior and inferior portions seperated by petinate line
  • S/I rectal arties/veins
    • internal hemorrhoids - superior rectal vein
    • external hemorrhoids - inferior rectal vein
93
Q

What are the borders of the lesser omentum?

A
  • epiploic foramen - opening to lesser sac
  • Gastrosplinic ligament
    • attaches stomach and spleen together
  • Splenorenal ligament
    • attaches spleen and kidneys together
94
Q

What is the bare area of the liver?

A
  • where there is no periotenium
    • made up of the r/l triangular ligaments
95
Q

What is the renal blood supply?

A
  • Renal arteries come off of the aorta at the level of the SMA
    • divide into anterior and posterior segmental branches as it reaches hilum
  • can be polar branches
  • left kidney has collateral blood flow, right doe snot
96
Q

What is the renal drainage?

A
  • Renal veins to the IVC
    • left is longer and has to pass under the SMA
97
Q

What are the three sites where the ureter narrows?

A
  • renal pelvis to ureter
  • pelvic brim
  • entrance to the bladder (enters diagonally)
98
Q

Innervation of kidneys

A
  • sympathetics from lesser and least and lumbar splanchnics
    • synapse in ganglia
  • Parasympathetics come from pelvic splanchnics, vagus and synapse in renal sinus
  • sensory fibers from kidneys
    • vagus
    • sympathetics
  • Sensory fibers from ureters
    • similar as kidneys but can return to DRG via T12-L2 spinal nerves as the pain can move down the ureter
99
Q

What is the blood supply to the supradrenal glands?

A
  • Superior suprarenal off inferior phrenic
  • middle suprarenal directly off aorta
  • inferior suprarenal off renal
100
Q

What is the innervation to the adrenal gland?

A
  • Only just one neuron
    • preganglionic sympathetic fibers innervate secretory cells
  • cells respond to stimulation by secreting epinephrine adn norepinephrine
101
Q

Describe hypogastric nerves

A
  • where the pre-vertebral ganglia split, arise from superior hypgastric plexus and supply inferior plexus
  • contains
    • ascending and descending nerves
    • afferents
    • parasympathetics (from pelvic nerves reaching colon)
102
Q

Identify these muscles

A
  • yellow - quadratus lumborum
  • green - psoas major
103
Q

Identify

A
104
Q

Name the branches off the aorta

A
  • inferior phrenics
  • celiac trunk
    • common hepatic artery, splenic artery, left gastric artery
  • middle suprarenal
  • SMA
  • renal
  • gonadal
  • IMA
  • numberous lumbar arteries
  • common iliacs
  • median sacral artery
105
Q

identify

A
  • middle white area with hole - central tendinous area
  • muscular part of diaphragm - peripheral muscular area
  • black line - medial arcuate ligament
    • where diaphragm abuts psoas major muscle
  • yellow line - lateral arcuate ligament
  • blue line - crura
106
Q

The esophagus opening is usually formed entirely by fibers from

A

right crus

107
Q

Lumbocostal trigone

A
  • Defect in the diaphragm, normally posterior later
  • formed by imcomplete closure of pericardioperitoneal canals by pleuroperitoneal membrane
    • can cause a congential diaphragmatic hernia
108
Q

What are the four embryonic structures that the diaphragm comes from?

A
  • Septum transversum
  • pleuroperitoneal membranes
  • dorsal mesentery from esophagus forms crura
  • body wall from cervical somites
109
Q

What is Cholelithiasis?

A
  • prescence of gall stones
  • fat, fertile, female, forty
  • Diagnosis
    • Ultrasound
110
Q

What is biliary colic?

A
  • occurs when the gallstones move
  • symptoms
    • intermittent upper right quadrant pain
    • lasts few mins to hours
    • occurs aftter eating fatty, greasy meal
  • more frequent the attacks the higher the risk of complications
111
Q

What is cholecystitis?

A
  • inflammation of gallbladder - acute or chronic
  • calculus vs. acalculous cholecystitis
    • gallstones cause 80-90% of acute cholecystitis
    • treatment is the same
  • worse the inflmmation, the higher the risk of complication
  • Diagnosis
    • ongoing pain in RUQ
    • Elevated LFTs
    • Ultrasound findings
112
Q

How is a pancreatitis diagnosed?

A
  • same as cholecysititis
  • Labs: amylase, lipase
  • Imaging
    • CT scan
    • MRCP
    • ERCP
113
Q

What is Ranson’s creiteria?

A
  • Acutely
    • age in years >70
    • WBC > 18000 cells/mm3
    • Blood glucose > 12.2 mmol/L (>220 mg/dl)
    • Serum AST >250 IU/L
    • Serum LDH > 400 IU/L
  • Score 0 to 2 - 2% mortality
  • Score 3-4 15%
  • Score 5 to 6 40%
  • Score 7 to 8 100%
114
Q

What is cholangitis?

A
  • primary
    • chronic autoimmune disease affecting the extra and intrahepatic bile ducts
    • leads to cirrhosis requiring liver transplant
  • Ascending
    • infection of common bile duct from obstrcutions
    • Charcots triad: fever, RUQabd pain, jaundice
    • Reynolds pentad - plus confusion and hyptension
    • treatment is immediate ERCP sphincterotomy after resuscitation and antibiotics
115
Q

Name theses posterior wall nerves

A
116
Q

What is the oxidative branch of PPP?

A
  • G6P -> ribulose 5-phosphate
    • G6P DeH
  • Generates NADPH
  • Generates biosynthetic precursors (ribulose 5-phosphate)
117
Q

What is the non-oxidative branch PPP?

A
  • ribulose 5-P -> 2x F6P or G3P
    • transketolase/transaldolase
    • TPP dependent

Block 3 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions