Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MET2 > MET2 Revision1 > Flashcards

MET2 Revision1 Flashcards

1
Q

What is the CT like in liver?

A
  • Very little
  • Sinusoids are supported by collagen type III
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Liver lobule structure:

What are the 3 zones in a liver lobule? [3]

Where are the 3 zones located in relation ot the portal triAd?

Differences in appearance between the 3 zones? [3]

A

Liver lobule structure:

All have different metabolic activities

What are the 3 zones in a liver lobule? [3]
* Zone 1: oxygenated blood
* Zone 2: medium oxygenated blood
* Zone 3: less oxygenated blood

Where are the 3 zones located in relation ot the portal triAd?
Zone 1: closest to portal triad: lighter purple
Zone 3: futhest to portal triad: deeper purple

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

What are the different functions of zone 1 c.f. zone 3 hepatocytes?

A

Zone 1 = oxidative/phase II reactions, gluconeogenesis and glycogen synthesis and, proteosynthesis and bile salt formation

Zone 3 = anaerobic/phase I reactions, glycogen stores (glycolysis), fat stores (lipolysis) and pigment store and glutamine synthesis

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

Describe how blood reaches the central vein

A

Blood from hepatic artery and portal vein mix and flow toward central vein through sinusoids

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

What is the name of the resident macrophages in the liver? [1]

Where exactly do they live? [1]

A

What is the name of the resident macrophages in the liver? [1]
Kupffer cells

Where exactly do they live? [1]
Lumen of sinusoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The gap between the endothelium and the hepatocytes is called WHAT? [1]

A

The gap between the endothelium and the hepatocytes = space of Disse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hepatocytes secrete bile into WHAT? [1]

A

Hepatocytes secrete bile into canaliculi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the passage of bile into gallbladder

A
  • Hepatocytes secrete bile into canaliculi
  • The canaliculi are defined by tight junctions between adjacent hepatocytes
  • Bile flows through these narrow tubes towards the hepatic (bile) duct
  • From the bile duct it flows into the biliary tree out of the liver to the gallbladder or intestines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the structure of gallbladder cells

A

Characteristic features:
* Irregular shaped villi
* Lined with very tall columnar epithelial cells
* Smooth muscle in the wall contracts under influence of hormone cholecystokinin
* Expels bile into duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Smooth muscle in the gall bladder wall contracts under influence of which hormone? [1]

Where is it secreted from? [1]

A

Smooth muscle in the gall bladder wall contracts under influence of hormone cholecystokinin: from duodenum

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

Which pro-inflam makers are produced when cirrhosis occurs? [3]

A

Chronic inflammation (TNF alpha, TGF beta, IL1 from Kupffer cells, endothelial cells, bile duct cells and hepatocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the histopathological changes that occur from steatosis (fatty liver disease)

A

Steatosis is the pathological retention of lipid in hepatocytes

Lipids accumulate in lipid droplets that can eventually displace the nucleus of hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Explain how alcoholism can induce steatosis?

A

Alcoholism can also induce steatosis because the metabolism of ethanol produces NADH which shifts the metabolism of hepatocytes toward lipid synthesis

  • Hepatocyte swelling and necrosis
  • If chronic then fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the histopathological changes that occur from cholestasis and why they occur [2]

A

Cholestasis is a pathological accumulation of bile within the liver parenchyma

It results from blockage of bile ducts or defects in bile secretion by hepatocytes

In this image, note the presence of bile in the ducts and cytoplasm of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are cholelithiasis? [1]

A

Gall stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are cholelithiasis / gall stones made from:

  • 80% of time
  • 20% of time
A

What are cholelithiasis / gall stones made from:

  • 80% of time: cholesterol stones
  • 20% of time: pigment stones: bilirubin calcium salts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Explain the MoA of insulin secretion from B cells

A

Glucose enters the β-cells

Glucokinase acts as the glucose sensor

Increased ATP/ADP ratio closes the ATP-sensitive potassium channel leading to depolarisation of the plasma membrane

This opens the voltage-gated calcium channel. The increase of intracellular calcium triggers secretion of insulin-containing granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Name other signals that can potentiate the insulin other than last slide [6]

A
  1. Intracellular catobolsim of amino acids increases cellular ATP / ADP ratio (leucine, arginine)
  2. Fatty acids
  3. Glucagon like peptide 1 (GLP-1)
  4. Glucose-dependent insulinotropic
    peptide (GIP)
  5. PNS release of Ach
  6. CCK

(most require glucose for activation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is glucagon secretion stimulated by? [3]

What is glucagon secretion inhibited by? [5]

A

Stimulated:
* Low blood glucose conc
* Increased blood A.A (especially alanine and arginine)
* Exercise

Inhibited:
* Hyperglycaemia
* GLP-1
* Somatostatin
* Insulin
* Zinc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Explain MoA of glucagon working
- Which type of receptor does it bind to?

A
  • Glucagon receptor is a GPCR
  • Upon ligand bonding, GTP displaces GDP on the a subunit. A subunit binds to the adenyly cyclase protein to activate
  • Causes activation of Adenyly Cyclase pathway
    (pathway is a key signalling cascade activated by glucagon).
  • Causes synthesis of cAMP as a second messenger (v important!) which actiavtes protein kinase A causes phosphorylation of enzymes used for reactions to make glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does insulin switch off glucagon dependent signaliing?

A

Phosphodiesterase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Effect of glucagon on [4]

glycogenlysis
glycogensis

At the liver: gluconeogenesis
glycolysis

A

Glucagon increases glycogenolysis
Glucagon inhibits glycogenesis

AND

At the liver: Inhibits glycolysis and increases GNG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the effect of glucagon on precursors for GNG?

COME BACK

A

Glucagon increases amino acids, lactate, and glycerol intake by hepatic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Role of catecholamines (in particular adrenaline) with regards to hypoglycaemia

A

Fight or flight x

E.g. Adrenaline:
It also acts as an insulin counter-regulatory hormone in response to hypoglycaemia

It signals via a G protein-coupled receptor: produces cAMP and causes activation of PKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Catecholamines monoamines (Dopamine, norepinephrine, and epinephrine) are synthesised from which two molecules? [2] Where? [1]
Adrenaline synthesised from **Phenylalanine** and **Tyrosine** At: **chromaffin** cells of the **adrenal medulla**
26
Effect of cortisol in: a) the liver [2] b) the muscle [2] c) adipocytes [2]
(opposite of insulin; similar to glucagon) In the liver: * **enhances gluconeogenesis** * **inhibits glycogen synthesis** In muscle: * **inhibits glucose uptake/utilisation** * **stimulates protein degradation** In adipocytes: * it stimulates **lipolysis** * **Rapid mobilisation of glucogenic amino acids and glycerol/fatty acids from cellular stores**
27
Growth hormone is stimulated by the release of which hormone? [1] Growth hormone is inhibited by the release of which hormone? [1]
Growth hormone: - stimulated by **growth hormone-releasing hormone** (**GHRH**) - inhibited by **somatostatin** (**SSTN**)  
28
What are the metabolic effects of growth hormone at: a) liver [2] b) sk. muscle c) adipose tissue
What are the metabolic effects of growth hormone at: a) adipose tissue: * **reduces lipogenesis** * **Increases lipolysis** * Overall effect: reduces body fat mass b) sk. muscle * **Reduces glucose uptake** * **Increases b oxidation** c) liver: * **increases production and uptake of IDL, LDL and HDL**
29
What is the effect of growth hormone on IGF-1? What is the effect of IGF=1 activated? [2]
IGF1 = Insulin-like growth factor 1 GH is a regulator of IGF1, specifically it **decreases renal GNG** and **increases glucose transport**
30
Thyroid hormone release causes increased basal metabolic rate. Explain how [3]
**Increase in the number and activity of mitochondria** * Increases the rate of ATP synthesis **Stimulation of carbohydrate metabolism** * Rapid glucose uptake * Enhanced glycolysis and gluconeogenesis * Increased insulin secretion **Stimulation of fat metabolism** * Lipids mobilised rapidly from fat tissue * Increased fatty acids concentration in the plasma
31
What are incretins? Name an important one
Incretins are a group of gastrointestinal hormones **GLP-1** (glucaon like peptide)
32
Effect of glucagon on fatty acid Beta oxidation and de novo lipogensis [2]
Glucagon **increases** fatty acids β oxidation Glucagon **inhibits** de novo lipogenesis
33
Growth hormone acts by activating which two receptors?
GH acts via **Growth Hormone receptor** [1] and **Prolactin receptor** [1]
34
Growth Hormone receptor is what type of specific receptor? [1]
**GHR is a type I cytokine receptor** that lacks intrinsic kinase activity and requires recruitment of Tyrosine kinases to signal
35
Which part is AP and PP? [2]
36
The anterior part is derived from an upgrowth from the oral ectoderm of the primitive oral cavity called **[]**
The anterior pituitary is derived from an upgrowth from the oral ectoderm of the primitive oral cavity called **Rathke's pouch**
37
What are the three types of cells in the AP? [3] What are their differing roles?
**Acidophil:** * Pink cytoplasm and dark nuclei * Secrete protein hormones: **growth factor and prolactin** **Basophils** * Purple cytoplasm * Secrete glycoprotein hormones: **adrenocorticotrophic hormone, thyroid stimulating hormone, follicle stimulating hormone and luteinizing hormone** Chromophobe * Non secretory serve as support or **precursors** for acidophils and basophils
38
What are the types of capillaries in the AP? [1]
The capillaries in this gland are **fenestrated**, to enable passage of hormones from the secretory cells into the bloodstream.
39
Which AP cells are which on the masson trichrome? [2]
40
Posterior Pit:
41
The **[]** portal circulation carries releasing hormones from the **[]** to the **[]** targeting the **[]** and **[]** and causing release of hormones into the blood stream.
the **hypophyseal** portal circulation carries releasing hormones from the **hypothalamus** to the **adenohypophysis** targeting the **acidophils** and **basophils** and causing release of hormones into the blood stream.
42
The bulk of the PP consists of axons from neurons in the [] and [] nuclei of the hypothalamus
The bulk of the PP consists of axons from neurons in the **supraoptic** and **paraventricular** nuclei of the hypothalamus
43
Label A of PP
Herring Bodies
44
What are the 3 divisions of the adrenal cortex? [3]
* Glomerulosa (near capsule) * Fasiculata * Reticularis (near medulla)
45
What are the cells of the adrenal medulla called? [1] What do they produce? [1]
What are the cells of the adrenal medulla called? [1] **Chromaffin cells** What do they produce? [1] catecholamines (**adrenaline and noradrenaline)**
46
How would an adenoma affect adrenal cortex?
* Adenoma = a benign tumour of glandular origin - e.g. increase in cortisol
47
What is pheochromocytoma? Name 3 symptoms
* Grows from the **chromaffin cells** * Most are benign only about 10% metastasise to other parts of the body * Very rare (8 people per 1 million) * Classic triad of episodic (in around 30%) * **Headaches** * **Sweating** * **Tachycardia** due to increased adrenaline release * Fine granular cytoplasm can be deeply basophilic * Granules are filled with catecholamines * Nuclei round or oval with one or more nucleoli
48
Label A1 and A2 B C
A1: Follicles A2: colloid (and a central mass of follicles) B: Follicular epithelial cells C: LCT
49
Why do follicular epithelial cells change in shape and how does this occur? [2]
Follicular cells - are almost columnar in appearance in some regions, whilst elsewhere they have a low cuboidal appearance. This is because in active glands, the follicles are smaller, and have reduced colloid - the cuboidal lining cells are relatively tall because they are actively making and secreting hormones - so packed full of ER and golgi. **Hypothyroidism = squamous or cuboidal Hyperthyroidism = columnar**
50
Explain characterisitcs of Hashimoto thyroidosis
* Autoimmune disease of T * Causes **hypothyrodism** due to destruction of TSH receptor * **Lympocyte** infiltration occurs
51
Identify the clusters of chief cells (CC), which secrete PTH. Also, identify oxyphil cells (OC), which are larger and paler staining than the chief cells.
52
What is the role of D-cells in islet of langehans? [1]
What is the role of D-cells in islet of langehans? **Produce somatostatin broad effects on gastrointestinal function, inhibits insulin and glucagon secretion**
53
Which of the following is the thyrocervical trunk? [1]
48
54
Label A-C of the liver
55
Which liver pathology is occurring here? [1]
cholestasis
56
Liver injury with cholestasis typically results in an increase of what laboratory value? Alanine aminotransferase Albumin Alkaline phosphatase Aspartate aminotransferase
Liver injury with cholestasis typically results in an increase of what laboratory value? Alanine aminotransferase Albumin **Alkaline phosphatase** Aspartate aminotransferase
57
What is this adrenal histopathology depicted? [1]
Pheochromocytoma
58
What is this adrenal histopathology depicted
Adrenalectomy with **pheochromocytoma**. Thin fibrous bands impart a nested look to pheochromocytoma.
59
Name this liver disease [1]
steatosis
60
A 60 year old man was admitted with massive hematemesis and hypovolemic shock. He failed to respond to resuscitation. Postmortem examination revealed a liver shown as above. What is the most likely cause of his massive gastrointestinal bleeding? Acute gastritis Aortoesophageal fistula Esophageal varices Hepatocellular carcinoma Peptic ulcer
A 60 year old man was admitted with massive hematemesis and hypovolemic shock. He failed to respond to resuscitation. Postmortem examination revealed a liver shown as above. What is the most likely cause of his massive gastrointestinal bleeding? Acute gastritis Aortoesophageal fistula **Esophageal varices** Hepatocellular carcinoma Peptic ulcer
61
What is this liver pathology? [1]
cirrhosis
62
What is this liver pathology? [1]
63
What is this liver pathology?
**Chronic cholecystitis** characterized by gallbladder wall thickening secondary to muscularis hypertrophy, with a dilated Rokitansky-Aschoff sinus and adjacent transmural lymphoid aggregate.
64
What is this liver histology? [1]

MET2 (52 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions