Brainscape's Knowledge GenomeTM

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


See full index

Endocrinology > Week 1 > Flashcards

Week 1 Flashcards

1
Q

what are the basic hormone subtypes

A

protein and peptide hromones, steroid hormoones and tyrosine derivatives

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

what are the hormones receptors

A

G-protein coupled receptors
Receptor Tyrosine Kinase (RTK) Families
Receptors associated with tyrosine kinase activity
Steroid hormone receptors

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

what are the major endocrine glands?

A

hypothalamus, PG, 4Parathyroid and thyroid, 2 adrenal glands and pancreas, ovaries/testes, adipose tissue

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

where do most clinical problems from endocrine come from?

A

hypo/hypersecretion

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

what are the principles of endocrine testing?

A

If too little hormone – try and stimulate it

If too much hormone – try and suppress it

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

what type of glands make up the endocrine system

A

ductless glands

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

how is communication (long distance between glands and other tissues) done in endocrine system?

A

via hormones in bloodstream

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

how are hormones are specific at signalling?(3 reasons)

A
  1. chemically distinct hormones
  2. specific receptor for each hormone
  3. distinct distribution of receptors across target cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the chemical nature and deriviative of Adrenaline + thyroid hormones (T3 and T4)?

A

modifed Amino Acids (from tyrosine)

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

what is the chemical nature and derivative of Cortisol, progesterone, testosterone?

A

steroid (from cholesterol)

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

what is the chemical nature and derivative of Adrenocorticotropic hormone ACTH), antidiuretic hormone (ADH), oxytocin?

(insulin)

A

peptide (from larger precursor proteins)

proteins

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

what are the three ways of chemical signally hormones can do?

A

autocrine, paracrine, endocrine

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

autocrine signalling definition

A

cell secretes a hormone or chemical messenger (called the autocrine agent) that binds to autocrine receptors on that same cell, leading to changes in the cell/INTRACELLULAR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

paracrine signalling definition

A

signalling molecule affects surrounding target cells (diffusion in ECF)

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

endocrine definiton

A

signalling molecule enters circulation and affects cells at a different site.

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

not all hormones act in one way. Somatostatin acts via which two signalling methods?

A

paracrine and endocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

one hormone can affect many targets and several H may act on one target. T or F?

A

T

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

why does a very small change in the concentration of H lead to changes?

A

due to specific receptors with high efficacy

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

how long does it take H to act? What can occur when H attaches to receptor?

A

seconds to days.

Amplification - cascade of events

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

how are H eliminated?

A

terminated by enzyme-mediated metabolic inactivation in the liver.

or at sites of action.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What two ways can hormones interact? (Give example of each)

A

complementary (together - adrenaline, glucagon and cortisol allow enhances physical activity and inc energy while preventing hypokalaemia and hypoglycaemia prophylactically)

antagonistically (in opposition - insulin and glucagon)

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

Amines: synthesis, storage, release and transport

A

pre-synthesised from tyrosine, storage in vesicle by adrenaline, release due to external factor causing inc extracellular Ca2+ - release on demand, always reserve.

as amines are small, soluble and hydrophilic they are transported ‘freely’ in bloodstream.

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

peptide H: synthesis, storage, release and transport

A

pre-synthesised by long processes (by CONVERTASES), storage in vesicles, release due to external factor causing inc extracellular Ca2+ - release on demand, always reserve.

peptide H are hydrophilic so they are transported/dissolve ‘freely’ in plasma

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

Steroid H: synthesis, storage, release and transport

A

synthesised and secreted on demand (no storage)

pathways irrelevant but all via PREGNENOLONE.

hydrophobic so transported by carrier proteins in plasma(CP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the rate limiting steps in Steroid H synthesis? (what inc steroid H synthesis)

A

(high) conc of cholesterol

(high) rate of conversion of cholesterol into pregnenolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

when are steroid H biologically active?

A

when ‘free’/when not bound to plasma proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what H are relatively insoluble in plasma?

A

steroids, T3, T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

T3 is what?

A

Triiodothyronine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

T4 is what?

A

Thyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the function of CPs? (give 3)

A

inc conc of H in blood

provide reservoir of H

to extend the T1/2 of H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

give examples of common CP

A

CBG - cortisol binding globulin (binds cortisol, some aldosterone)

TBG - binds T4, some T3.

SSBG - testosterone + oestradiol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are two important general CP and what do they carry?

A

albumin – binds many steroids and thyroxine

transthyretin – binds thyroxine and some steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how does CP regulate levels of steroid H?

A

acts as both buffer and reservoir (equilibrium between CP bonded and non-bonded). If too much or too little steered body can cope.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what state do H have to be to cross capillary wall (and nuclear membrane?)

A

free (unbonded)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how is H plasma conc levels maintained?

A

negative feedback system (both short range and long range)

[note that nervous and endocrine systems work together]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is plasma concentration determined by?

A

rate of secretion vs rate of elimination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

neuroendocrine in negative feedback system?

A

Elicits a sudden burst in secretion in response to a specific stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is diurnal/circadian rhythm?

A

fluctuation thoughtout day [dependant on external factors e.g:night/day]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the two main route of H elimination?

A

excretion by kidneys

metabolism by liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are the half life (approx) of amines, peptides and steroid H?

A

amine - secs
peptides-min
steroid-hours/days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

3 types of H receptors?

A

G-protein coupled (GPCR)
Receptor kinases
Nuclear receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

G-protein receptors: are found where, which H use them?

A

found on cell surface as hydrophilic H

amine H and some peptide H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

receptor kinases: are found where, which H use them?

A

found on cell surface as hydrophilic H

activated by some protein/peptide H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

nuclear receptors: classes, are found where, which H use them?

A

receptor on nucleus as lipophilic H (can diffuse across PM)

Class 1 - many steered H; located in cytoplasm and move to nucleus when activated
Class 2 - mostly lipids; constitutively present in the nucleus
Hybrid - activated by thyroid hormone (T3) and other substances; similar in function to class 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the difference between type 1 and 2 diabetes?

A

1- absolute insulin deficiency

2-relative insulin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is the definition of DM?

A

a group of metabolic diseases characterised by hyperglycemia resulting from defects in insulin secretion, insulin action, or both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

how is diabetes diagnosed?

A

HbA1c > 48m/m/6.5% (type 2)

fasting glucose >7mmol/L

2hr glucose in OGTT > 11.1mmol/L (after 2hrs)

random glucose>11.1mmol/L (=symptoms)
[slightly lower values can indicate pre-diabetes /impaired function]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

type 1 DM PC

A 
Pre-school and peri-puberty
Small peak in late 30’s
Usually lean
Acute Onset
severe symptoms
severe weight loss
ketonuria  metabolic acidosis
no evidence of microvascular disease at diagnosis
immediate and permanent requirement for insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what signs to look out for in type 1 DM?

A

4T’s

toilet, thirsty, tired, thinner

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

type 2 DM PC

A

middle-aged/elderly
usually obese
pre-diagnosis duration of probably 6-10 years
insidious onset over weeks to years
ketonuria minimal or absent
evidence of microvascular disease at diagnosis in 20 %
managed initially with diet/ lifestyle +tablets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

risk factors for type 2 DM

A 
Obesity (central)
Family History
Gestational Diabetes
Age
Ethnicity (Asian, African, Afro-Caribbean)
PHx of MI/ Stroke
Medications e.g. antipsychotics
IGT/ IFG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is mostly likely cause of DM in children under 1?

A

neonatal or genetic diabetes

rarely type 1 (even if looks like it)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

type 1 DM is what kind of disease? what occurs? what does this allow to help in diagnosis?

A

AID, insulitis (lymphocytic inflitrate). Antibodies can be used to diagnoses as AID.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

PC of type 2 DM

A 
Thirst 
Polyuria
Thrush
Weakness Fatigue
Blurred Vision
Infections
(Weight Loss)
T2DM- Signs of complications- neuropathy, retinopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what are useful discriminatory tests (tell you which type of diabetes is present)?

A

GAD/ Anti-Islet Cell antibodies

Ketones

C-peptide (plasma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what is LADA?

A

Latent autoimmune diabetes (type 1 occuring in adults).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

lots of patients with LADA are assumed to have type 2 DM. how is LADA different?

A

ketosis = type 1 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

type 3 diabetes causes are what?

A

pancreatic disease, endocrine disease, drug-induced, Abnormalities of insulin and its receptor,
Genetic diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what pancreatic conditions cause type 3 diabetes?

A

Chronic or recurrent pancreatitis (alcoholism mainly)
Haemochromatosis
Cystic Fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what endocrine conditions cause type 3 diabetes?

A

Cushing’s syndrome
Acromegaly
Phaechromocytoma
glucagonoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what drugs

cause type 3 diabetes?

A

Glucocorticoids
Diuretics
B-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what genetic disease cause type 3 diabetes?

A

Cystic fibrosis
Myotonic dystrophy
Turner’s syndrome
Down’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what are signs of monogenic diabetes (not polygenic)?

A 
Strong Family History
Associated Features (renal cysts etc)
Young Onset
GAD-negative
C-peptide positive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what is type 4 DM?

A

Gestational diabetes - Any degree of glucose intolerance arising or diagnosed during pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what is HbA1c? what is its use?

A

Glycated haemoglobin.

Provides a measure of glucose control over past 2-3 months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

complication of DM

A

Macro-vascular: Heart Disease and Stroke (70% of people with diabetes die from cardiovascular disease)

Micro-vascular: Retinopathy(blindness), Nephropathy (RF), Neuropathy,

Psychiatry/ Psychology

Peripheral vascular disease - ulcers/amputation

DKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what is DAFNE?

A

dose adjustment for normal eating (type 1DM)

[educates people on estimating carbohydrate per meal and injecting the right does of insulin]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

which DM has stronger genetic competent?

A

type 2 (twin studies and risk factor for type 2 development greater if parents have than type 1 - weird)- extra info

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what is a normal blood glucose level?

A

5mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what are the cells of the pancreatic islets, watch percentage and what do they produce?

A

β cells - secrete insulin (70%)
α cells - secrete glucagon (15%)
δ cells - secrete somatostatin (5%)
PP cells - secrete pancreatic polypeptide (<1%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

how is insulin made? (?→?+?→?+?)

A

preproinsulin→ proinsulin +singalling petpide →insulin + C-peptide (cleaved to form insulin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

where is preproinsulin made?

A

Synthesized in the rough endoplasmic reticulum of pancreatic β cells [as a larger single chain preprohormone]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

how fast can insulin preparations work?

A

ultra-short acting to ultra-long acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

ultra-short acting insulin called what? taken when?

A

lispro.

Injected within 15 minutes of beginning a meal
short duration of action- must be used in
combination with longer-acting preparation for Type 1 diabetes unless used for continuous infusion
(it is monomeric and not antigenic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

ultra-long acting insulin called what? when is it given?

A

glargine

Recombinant insulin analog that precipitates in the neutral environment of subcutaneous tissue
Peakless- prolonged action
Administered as single bedtime dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

how does glucose enter the Beta-cells?

A

GLUT2 glucose transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what happens to glucose once it enters the beta-cell?

A

it is phosphorylated by glucokinase (glucokinase is the glucose-sensor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what can lead to dramatic change in glucokinase captivity?

A

(small) change in glucose conc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what is the process for excreting insulin?

A

inc metabolism of glucose→ inc intracelluar ATP conc →inhibition of ATP-sensitive K+ channels Katp → depolarisation of cell membrane → opening of voltage- gated Ca2+ channels → inc intracellular Ca2+ → fusion of secretory vesicles with the cell membrane and release of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

how many cells make and secrete insulin?

A

ONLY B-cells make and secrete

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

when should insulin be secreted?

A

ONLY once conc > 5mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the problem in Type 1DM, …type 2 DM?

A

B-cells are lost -1

cells lose ability to sense change in glucose. - 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what is the release of insulin? Why?

A

biphasic → readily released pool (immediate ) and reserve pool (preparation reaction must occur)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what happens to the insulin secretion curve in Type 2 DM?

A

it flattens and weakens (due to down regulation of sensory process)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what drugs can mimic the action of ATP to depolarise beta cells?

A

sulphonylurea drugs [SUR’s]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what do Katp channels consist of which two proteins?

A

Kir6 (An inward rectifier subunit (Kir) - pore subunit )

SUR1 (A sulphonylurea receptor - regulatory subunit) - need both to form functional Katp channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what is the structure of Katp channel?

A

octomeric structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

how to SUR’s work?

A

directly inhibit Katp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

give some example of SUR’s, when can they be used?

A

tolbutamide or glibenclamide

2nd line for type 2 DM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

how is Katp regulated?

A

inhibited by SUR’s (stimulates insulin secretion)

stimulated by diazoxide (inhibits insulin secretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what mutation give neonatal diabetes?

A

Kir6.2 mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

why does neonatal diabetes occur? treatment?

A

Due to constitutively activated KATP channels or an increase in KATP numbers

In some of these patients the β cells are usually responsive to SURs, such as tolbutamide; recover euglyceamia fairly quickly on SURs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what does euglyceamia mean?

A

normal blood glucose (normoglycemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

what mutations lead to congenital hyperinsulinism?

A

some Kir6.2 or SUR1 mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

why does congenital hyperinsulinism occur? treatment?

A

trafficking or inhibiting mutations

diazoxide can help inhibit insulin secretion if channels are still getting to the membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

MODY: what is it? who does it occur?

A

Maturity-onset diabetes of the young

Monogenic diabetes with genetic defect in β cell function; Familial form of early-onset type II diabetes, primary defects in insulin secretion

Mutations in at least 6 different genes can cause MODY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

why is it important to differentiate MODY from type 1 DM? how is this done?

A

treatment with sulphonylurea rather than insulin (as MODY patients usually have some b-cell function available).

robust genetic screening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what occurs in type 1, 2 and MODY?

A

Type 1 Diabetes – Loss of insulin secreting beta cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what occurs in type 2 DM

A

Type 2 Diabetes- Initially hyperglycemia with hyperinsulinemia so primary problem is reduced insulin sensitivity in tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what occurs in MODY?

A

MODY- defective glucose sensing in the pancreas and/or loss of insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what is insulin’s biological effect

A

anabolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

what does insulin promote?

A
  • Amino acid uptake in muscle
  • DNA synthesis
  • Protein synthesis
  • Growth responses
  • Glucose uptake in muscle and adipose tissue
  • Lipogenesis in adipose tissue and liver
  • Glycogen synthesis in liver and muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

what does insulin inhibit?

A

lipolysis

gluconeogenesis in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what receptor does insulin bind to?

A

receptor tyrosine kinases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

what does insulin cause to happen at the tyrosine kinase receptor?

A

insulin binds to α subunits → β subunits to dimerise → β + phosphorylate themselves/autophosphorylation → activates catalytic activity of the receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

how does glucose get transported into the cell?

A

GLUT 4 receptor (then glycogen synthesis occurs as does cell growth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

what is insulin resistance?

A

reduced ability to respond to ‘physiological’ insulin levels - due to reduced insulin sensing and/or signalling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

what is the effect of obesity/adipose tissue on insulin resistance?

A

direct correlation with obesity
[however complete absence of adipose also results in insulin resistance] (therefore adipose tissue is key mediator of insulin sensitivity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

what is leprechaunism/Donoghue syndrome? why does it occur?

A

Rare autosomal recessive condition, mutations in the gene for the insulin receptor causes severe insulin resistance. [defects in insulin binding or insulin receptor signalling]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

what type of condition is type 2 DM? (genetically)

A

polygenic, [with a large input from environmental influence]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

leprechaunism/Donoghue syndrome signs?

A

Developmental abnormalities (elfin facial appearance,
growth retardation,
absence of subcutaneous fat, decreased muscle mass) - death < 1yearold.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

genetics of Rabson Mendenhall syndrome?

A

Rare autosomal recessive condition,

113
Q

what is Rabson Mendenhall syndrome?

A

Severe insulin resistance, hyperglycemia and compensatory hyperinsulinemia

114
Q

signs of Rabson Mendenhall syndrome

A

Developmental abnormalities

Acanthosis nigricans (hyperpigmentation)

Fasting hypoglycaemia (due to hyperinsulinemia)

DKA

115
Q

DKA PC

A 
Vomiting
Dehydration
abdo pain
deep gasping breaths
confusion/unconsciousness
Increased heart rate
Distinctive smell on breath
116
Q

where are ketone bodies formed?

A

liver mitochondria. [then diffuse into bloodstream and to peripheral tissues]

117
Q

what are ketone bodies derived from?

A

acetyl-CoA, which is from β oxidation of fats.

118
Q

what are ketone bodies good for/used for by body?

A

Important molecules of energy metabolism for heart muscle and renal cortex (converted back to acetyl-CoA, which enters TCA cycle)

Emergency energy
supply for brain
during fasting

119
Q

what inhibits lipolysis and prevents ketone body overload?

A

insulin (even small amounts)

120
Q

when can DKA occur?

A

T1DM - if miss insulin supplementation

T2DM -rarer (as there is still inhibition of lipolysis); can occur as insulin resistance and deficiency increases, alongside increase in glucagon.

121
Q

when is Acetyl CoA diverted to ketones in TCA cycle?

A

is supply of Oxaloacetate is limited.

122
Q

what does fatty acid oxidation yield?

A

acetyl-CoA → enters the TCA cycle if fat and carbohydrate degradation are balanced.

123
Q

why is Oxaloacetate consumed?

A

for gluconeogenesis

124
Q

give examples of ketone bodies

A

Acetone
Acetoacetic acid
β-hydroxybutyric acid

125
Q

when glucose is not available, what are oxidised to provide energy

A

fatty acids.

126
Q

what happens to the excess acetyl-CoA in a low glucose environment?

A

Excess acetyl-CoA is converted to ketone bodies, blood levels increase.

127
Q

what does the accumulation of ketone bodies in blood lead to?

A

acidosis (metabolic)

128
Q

what does high glucose excretion cause?

A

dehydration, exacerbates acidosis

129
Q

what is severe complication of DKA

A

coma, death

130
Q

how is DKA treated?

A

insulin (and rehydration)

131
Q

what conditions does ketosis occur?

A

glucose limiting conditions (starvation and diabetes).

132
Q

what are the four parts of the brain?

A

cerebral hemispheres, cerebellum, brainstem, spinal cord

133
Q

what makes up the Diencephalon

A

Thalamus (T) + Hypothalamus (H)

134
Q

where is the diencephalon

A

onto of midbrain of brainstem.

135
Q

how is the hypothalamus anatomically & functionally connected to the pituitary gland?

A

infundibulum or “pituitary stalk”

136
Q

which bone does the pituitary fossa lie in?

A

sphenoid bone (within sella turcica)

137
Q

what effect can a PG tumour have on the visual pathway? why

A

can cause Bitemporal hemianopia (loss of temporal field of view); because pitc chaism is impinged

138
Q

what are the two way to surgically access the PG?

A

Transcranial approach (subfrontal – under the frontal lobe)

transphenoidal approach (via nasal cavities & sphenoid sinus)

139
Q

what two concha contribute to the ethmoid bone? which is a bone in its own right

A

Inferior concha = bone on its own;

Sup and middle concha part of ethmoid bone

140
Q

what are the paranasal sinuses? what types are there?

A

Air-filled spaces within the bones surrounding the nasal cavities

Frontal bone (frontal sinuses)
Maxillae (maxillary sinuses)
Ethmoid bone (ethmoidal air cells) - 3 groups
Sphenoid bone (sphenoid sinuses)
  • all R+L sinuses
141
Q

possible function of paranasal sinuses

A

make mucus and drain it into nasal cavities, reduced weight of skull, add resonance to voice. (no real function?)

142
Q

what are paranasal sinuses lined by?

A

mucous-secreting respiratory mucosa

143
Q

which paranasal sinuses are important when concerned with PG?

A

sphenoid sinuses

144
Q

what does a transphenoidal transnasal approach involve

A

surgical fracture of the nasal septum and the floor (septum) & roof of the sphenoid sinus(es)

145
Q

what can be used by surgeons go gain access to PG in more complicated cases

A

Le Fort 1 Down-#

146
Q

which CN can be damaged in PG surgery causing eye problems?

A

CN3-6

147
Q

a Transcranial approach can lead to damage of what CN causing what?

A

Injury to CN1= reduced smell

148
Q

what is the dura mater?

A

thick layer that is outermost of 3 layers of meninges; adheres to the internal aspects of all the bone of the cranial vault

149
Q

what is the function of dural venous sinuses?

A

to drain blood from cranial cavity (inc brain) into the internal jugular veins. (not histologically veins but function like veins)

150
Q

what are two types of dural venous sinuses?

A

cavernous(R/L) and intercanvernous (A/P)

151
Q

what passes through the cavernous sinuses?

A

internal carotid artery

152
Q

what is the function and function deficit of optic chasm?

A

Conducts APs bilaterally from the nasal retinae

bitemporal hemianopia

153
Q

what is the function and function deficit of Oculomotor nerve

A

Motor to muscles that move the eyeball (globe)
Parasympathetic to the sphincter muscle of the iris

problems with several eye movements
a dilated pupil

154
Q

what is the function and function deficit of Trochlear nerve

A

Motor to one muscle that moves the globe

problems with specific eye movements

155
Q

what is the function and function deficit of Trigeminal nerve

A

Sensory to most of the face
Motor to the muscles of mastication

sensory symptoms on the face
difficulty chewing

156
Q

what is the function and function deficit of Abducent nerve

A

Motor to one muscle that moves the globe

problems with specific eye movements

157
Q

what is the function and function deficit of Cavernous sinus

A

Drains venous blood

venous haemorrage

158
Q

what is the function and function deficit of internal carotid artery

A

Supplies arterial blood to brain & orbit (including globe)

catastrophic haemorrage

159
Q

what is the function and function deficit of dura mater

A

Protects the structures of the cranial cavity

Cerebrospinal fluid (CSF) leak.

160
Q

thyroid gland consists of what? (anatomically)

A

2 lateral lobes (right & left) and an isthmus (a narrow connecting band)

161
Q

where do the lobes of the thyroid attach?

A

the lateral aspects of the thyroid & cricoid cartilages and to the trachea

162
Q

where does the isthmus lie?

A

lies anterior to the 2nd & 3rd cartilages of the trachea

163
Q

where are the 4 parathyroid glands located?

A

on the posterior surfaces of the thyroid gland’s lateral lobes (Sup and inf L+R)

164
Q

what is the pyramidal lobe? how may people have one? Where dos it commonly originate from? Where does it attach/extent to? Why?

A

anatomical variation coming of the thyroid (posterior) in 44% of people;commonly originates from left lateral lobe.

Most attach superiorly to thyroid cartilage; May extend as far superiorly as the hyoid bone (occurs as in embryology thyroid gland begins at junction of 2/3rd of tongue and migrates down via thyroglossal duct)

165
Q

what are the platysma muscles? what do they do? Nerve supply?

A
  • Located immediately deep to the skin within the superficial fascia of the neck
  • Belong to the group of muscles called “the muscles of facial expression”
  • Nerve supply is cranial nerve VII (the facial nerve)
166
Q

name the fascial compartments of the neck

A

pre-vertebral (deep), investing, 2 carotid sheaths, pre tracheal fascia.

167
Q

what is in the investing fascia?

A

Encloses all the other neck fascial compartments encloses 2 pairs of muscles:
Trapezius
Sternocleidomastoid

168
Q

what is in the prevertebra (deep) fascia?

A

Located posteriorly encloses:
Postural neck muscles
Cervical vertebrae

169
Q

what is in the pre tracheal fascia?

A 
Located anteriorly &amp; encloses: 
Oesophagus
Trachea
Thyroid gland
Strap muscles 
Recurrent laryngeal nerves
170
Q

what is in the 2 carotid sheaths?

A 
Located anterolaterally &amp; encloses:
Vagus nerves 
Deep cervical lymph nodes
Carotid arteries
Internal jugular vein
171
Q

where does the SCM attach?

A

Sternal head: attaches to the manubrium of the sternum

Clavicular head: attaches to the medial end of the clavicle

Both heads pass superiorly to attach to the mastoid process of the temporal bone

172
Q

what nerve supplies SCM & trapezius?

A

CNXI

173
Q

where does the trapezius attach (descending part)

A

Attaches inferiorly to the spine of the scapula & the lateral end of the clavicle

174
Q

where do the external and anterior jugular veins run?

A

within superficial fascia

Drain into subclavian and external jugular vein respectively

175
Q

where are the carotid sheaths located?

A

-Deep to the investing fascia -located anterolaterally in the neck either side of the thyroid gland
(they are bilateral tubes of deep fascia)

176
Q

what is enclosed within the carotid sheath?

A

IJV
Common + internal carotid arteries
Vagus nerve
Deep cervical lymph nodes

177
Q

what does carotid sheath do superior/inferior

A

sup= attach to base of skull

inf = blend with mediastinal fascia (infection spread easy to mediastinum)

178
Q

what is the arterial blood supply to the thyroid and parathyroid glands?

A

LV → arch of aorta → subclavian and common carotid → inferior and superior thyroid artery arise respectively. (have L+R inf and sup thyroid arteries).

also thyroid ima artery is anatomical variation what goes up cartilage to supply (may be nicked in emergency tracheostomy)

179
Q

what is the venous blood drainage from the thyroid and parathyroid glands?

A

have sup, middle and inf thyroid veins.

sup and middle → IJV → brachiocephalic veins →SVC

inferior right drains into mainly right brachiocephalic vein but sometimes left. Left always to left

180
Q

why is there a venous plexus around thyroid?

A

allows release of thyroid hormones

181
Q

lymphatics of thyroid/paratyhroid glands

A

superior deep cervical LN, inferior deep cervical LN, tracheal lymph nodes (Pretracheal node +
Paratracheal nodes)

ON RIGHT:Lymph is returned via the Right lymphatic duct to the Right venous angle

ON LEFT:Lymph is returned via the Thoracic duct
to the Left venous angle

182
Q

detail the vagus nerves (CNX) route through neck, throat to abdomen (wandering nerve)

A 
Branch from the medulla oblongata
Exit the skull via the jugular foramen
Descend through in carotid sheath
Descends through the chest:
Right CNX – Lateral to trachea
Left CNX – Left side of aortic arch
Both – Posterior to the lung hilum and on the oesophagus
Both vagus nerves pass through the diaphragm with the oesophagus

Then divide into their terminal branches on the surface of the stomach supply the abdominal organs with parasympathetic axons to the distal midgut

183
Q

what is the route of the left recurrent laryngeal nerve?

A

recurs (turns back in opposite direction) under the arch of the aorta (comes of L vagus)

184
Q

what is the route of the right recurrent laryngeal nerve?

A

recurs under the subclavian artery (comes of R vagus)

185
Q

what happens if recurrent laryngeal nerve damaged?

A

cannot move vocal cords so Lose abiity to produce acurrate sound/speak

186
Q

what are the 4 strap muscles? what are their fustiness

A

Superficial (omohyoid and sternohyoid )and deep (thyrohyoid, sternothryroid).

Move hyoid and thryoid up and down in swallowing

187
Q

which strap muscle has superior an inferior belly? why?

A

Omohyoid

Fascial sling attaching the intermediate tendon of omohyoid to the clavicle

188
Q

what are the surgical approaches to the thyroid gland?

A 
Classical thyroidectomy                         (similar approach to tracheostomy) - open
Endoscopically assisted thyroidectomy - keyhole
Endoscopic trans-axillary approach (armpit)
Endoscopic trans-breast approach (breast)
189
Q

what is the medical name for adam’s apple?

A

Laryngeal Prominence [of the Thyroid Cartilage]

190
Q

neck surface anatomy has two 4 key areas, what are they? (order from midline)- for right side of neck

A

right anterior triangle of the neck; SCM (with sternal + clavicular heads), right posterior triangle of the neck, trapezius

191
Q

where is the poster triangle of the neck located?

A

between SCM and trapezium

192
Q

where in anterior triangle of the neck?

A

between midline and SCM border - many important structures (carotid sheath, strap muscles)

193
Q

how is a Classical Thyroidectomy incision performed

A

Incision should be just superior to the clavicles & jugular notch; made through skin & platysma

“collar” incision made in natural ski crease or in direction of Langer’s lines

194
Q

what can easily be damaged in Thyroidectomy? how?

A

recurrent laryngeal nerve. Berry’s ligament needs cut (as attached thyroid to cartilage and RLN runs very close to berry’s ligament)

195
Q

what does the recurrent laryngeal nerve do?

A

provides somatic motor supply to most of the skeletal muscles that move the right vocal cord (the intrinsic muscles of the larynx)

196
Q

what does unilateral injury of recurrent laryngeal nerve cause?

A

“hoarseness” or weakness of the voice & a weak cough

197
Q

what does bilateral injury of recurrent laryngeal nerve cause?

A

aphonia (inability to produce sound)

inability to close the rima glottidis (opening between vocal cords) to prevent aspiration (inhalation of foreign body into the lungs) or to produce a good cough (requires closure of the rima glottidis)

198
Q

what is the rima glottidis

A

a space between the vocal cords

199
Q

what is berry’s ligament function?

A

attaches thyroid to cartilage

200
Q

what are the causes of death from DM?

A

coma, sepsis, vascular disease.

201
Q

what is the peak age of T1DM diagnosis?

A

9-12, also small peak early 30’s

202
Q

what is the aetiology and pathophysiology of Type 1 and 2? (what happens to the islet cells?)

A

lymphocytes infiltrate causing insulitis = type1

amyloid deposits cause fibrosis = type 2

203
Q

what genes cause type 1 DM

A

HLA and non-HLA (many types) can increase risk

204
Q

in which months in DM diagnosis rate raised?

A

Dec-Jan

205
Q

what antibodies are used for diagnoses type1DM

A

islet cell autoantibodies (ICA)

206
Q

what are the ICA antibodies?

A

GAD65(glutamic acid decarboxylase),
IA-2 (protein tyrosine phosphatase),
IAA(antibodies to insulin),
ZnT8 (zinc)

207
Q

what is Erythema ab igne

A

skin condition caused by long-term exposure to heat

208
Q

what is the trigger for AID type 1DM?

A

viral (weight and puberty then accelerate it)

209
Q

what are the disease markers in type 1 clinical diabetes

A

raised glucose, ketones are main signs

210
Q

what are the disease markers in type 1 pre-diabetes

A

Gad65, IA2 are main antibodies

211
Q

typical PC symptoms

A

Classic triad: -Polyuria [Enuresis in children], Polydipsia, Weight loss

Fatigue and somnolence
Blurred vision
Candidal infection: -Pruritis vulvae, Balanitis

keto-acidosis

212
Q

when do you hospitalise a new case of diabetes?

A

DKA, vomiting, significant ketonaemia

213
Q

what needs considered in social Hx

A
  • school, college or university?
  • employment
  • Does the individual drive?
214
Q

management of newly diagnoses Type 1DM

A

Blood glucose + ketone monitoring.

Insulin: usually basal [once daily] bolus [with meals] regimen + Carbohydrate estimation

Regular DSN and Dietitian contact

Appropriate medical clinic review: Weight, BP,
Bloods: HbA1c, Renal Function and Lipid; Retinal screening, Foot risk assessment

Record severe hypoglycaemic episodes or admission with diabetic ketoacidosis

215
Q

what are the complications of poor diabetes control?

A

Retinopathy
Nephropathy
Neuropathy

(HbA1c is good predictor)

216
Q

when is type 1 mot commonly diagnosed?

A

1-30

217
Q

when is type 2 most commonly diagnosed?

A

young adult-elderly

218
Q

when is MODY most commonly diagnosed?

A

13-30

219
Q

when is LADA most commonly diagnosed?

A

20-30’s

220
Q

when is secondary diabetes most commonly diagnosed

A

20+

221
Q

what is the pattern of normal insulin secretion?

A

Biphasic secretion in response to meal

  • Rapid phase of pre-formed insulin lasts 5 to 10 mins
  • Slow phase over 1 to 2 hours
222
Q

where is insulin secreted?

A

into portal vein

223
Q

what percentage of people with CF develop sedentary diabetes?

A

20%

224
Q

what is the likelihood of FHx for each type of diabetes? (1, 2, monogenic, secondary) in descending order of likelihood

A

Monogenic, 2, 1 ,secondary

225
Q

what is the likelihood of ketourea at presentation for each type of diabetes? (1, 2, monogenic, secondary)

A

type 1 +++, sceondary +, type2/monogenic = usually none

226
Q

what is the likelihood of weight loss at presentation for each type of diabetes? (1, 2, monogenic, secondary)

A

type 1 -usual, type2/monogenic-not usually, secondary = depends of cause

227
Q

what is the likelihood of complications at presentation for each type of diabetes? (1, 2, monogenic, secondary)

A

type 1 - never, type 2 - up to 30%

monogenic/secondary - unusual

228
Q

what is the typical age range of presentation for each type of diabetes? (1, 2, monogenic, secondary)

A

type1 - <5 and 10-14.
type2 - >25
monogenic - neonate to adulthood.
secondary - usually later in life

229
Q

what is the duration of symptoms pre-presentation for each type of diabetes? (1, 2, monogenic, secondary)

A

Type1 - short, severe
type2 - months, mild
monogneic - months, mild
secondary - weeks, depends on cause

230
Q

how to tell between type 1 + 2 DM?

A

age, BMI, symptoms, FHx of DM, ketones on urinalysis, glucose at presentation (>25 = type 1),

231
Q

when are you likely to suspect neonatal (monogenic) diabetes rather than type 1 DM

A

Children diagnosed under the age of six months are much more likely to have Monogenic rather than Type 1 Diabetes

232
Q

what does LADA stand for?

A

LAtent onset Diabetes of Adulthood (lowly progressing type 1/type1.5 DM).

233
Q

when to suspect LADA?

A

non-obese Male, 25-40

Auto-antibody positive, Associated auto-immune conditions

Non-insulin requiring at diagnosis, Sub-optimal control on oral agents

234
Q

patient with CF (random facts)

A

diabetes common, usually found in ‘severe’ mutations, i.e. ∆508, Prone to complications,
Insulin therapy preferred,
Screening with OGTT from age 10 years recommended.

235
Q

what does DIDMOAD ( or Wolfram Syndrome ) stand for?

A

diabetes insipidus, diabetes mellitus, optic atrophy, and deafness (also neurological anomalies)

236
Q

Bardet-Biedl Syndrome signs

A 
Often very obese
Polydactyly
Hypogonadal
Visual impairment
Hearing impairment
Mental retardation
Diabetes

Consanguineous parents

237
Q

distinguishing feature in type 1 DM diagnosis

A

Short/severe
Ketones+++
Abs POS

238
Q

distinguishing feature in type 2 DM diagnosis

A

Long/mild
Ketones 0
Abs NEG
Overweight

239
Q

distinguishing feature in MODY diagnosis

A

Variable
Ketones 0/+
Abs NEG
Inheritanc

240
Q

distinguishing feature in LADA diagnosis

A

Longer/variable
Ketones 0/++
Abs POS
Insulin delayed

241
Q

what are some relatively commonly associated AID’s with diabetes?

A 
Thyroid disease
Coeliac disease
Pernicious Anaemia
Addison’s disease
IgA deficiency
PolyglandularEndocrinopathy
242
Q

coeliac’s disease:PC + tests

A

Often asymptomatic
Bloating/diarrhoea
Malabsorption

Anaemia
Low albumin
Low calcium
Anti TTG Antibodies
NB IgA deficiency
Duodenal Biopsy
243
Q

thyroid disease: PC and tests

A

Many asymptomatic, Family History, Weight change, Deterioration in HbA1c, Hypoglycaemia

TSH
Consider Thyroid Abs

244
Q

what needs to be screened for in diabetics?

A

weight, BP, retinal scan, foot risk

245
Q

what test is used to regularly screen control of diabetes?

A

HbA1c, or glycerated haemoglobin

246
Q

treatment of type 1 DM

A

insulin, educate, DAFNE,

247
Q

aims of treatment of type 1 DM

A

prevent hyperglycaemia, avoid hyperglycaemia, reduced chronic complications

248
Q

hypergylcaemia signs/symptoms

A

Thirst, tiredness, blurred vision, weight loss, polyuria, nocturia, fungal infections

Cognitive, mood state, information processing, working memory

Potential risk of diabetic ketoacidosis (“DKA”)

249
Q

hypoglycaemia signs/symptoms

A

Pallor, sweating, tremor, palpitations, confusion, nausea, hunger.
Cognitive: tense-tiredness, information processing, working memory, coma

250
Q

chronic complications of DM

A

microvascular disease
macrovascular disease
Avoidance of acute metabolic complications – DKA, SHG
Reduced psychosocial morbidity

251
Q

what does a 1% reduction in HbA1c do?

A

lowers complications by 75%

252
Q

what does the basal bolus regime consist of?

A

basal - long-acting insulin
bolus - before meals insulin

(can add in more/alter if necessary)

253
Q

what is the twice daily regime

A

insulin taken twice a day (for elderly/non-compliant)

254
Q

what needs to be taken into account when administering insulin dose?

A

carbohydrate intake
exercise
alcohol
pre-meal glucose

255
Q

when is the one daily long-acting insulin does used?

A

severe type 2 DM

256
Q

most people with Type 1 treated in what two ways?

A

MDI (x3-4 injections per day) or CSII (continuous subcutaneous insulin infusion/insulin pump)

257
Q

what is the rule of thumb for starting insulin dosage?

A

0.3 units/kg body weight per day

258
Q

how are diabetics managed in hospital?

A

they control their own blood sugar/insulin therapy

259
Q

why are insulin regimes different from perosn to person

A

no one is the same - insulin rate of absorption differs,

route of administration preference, type of inulin/dosage variable

260
Q

how is control of diabetes measured? (at home and clinic)

A

home blood glucose monitoring (newer continuous glucose monitor)

HbA1c

(rarely use urine testing for glucose/ketones anymore)

261
Q

what is the advantage of continuous glucose monitoring over home glucose fingerstick tests?

A

“Fingerstick tests are like watching only a few scenes; CGM is like watching an entire movie. You get the full story.”

262
Q

what is the largest component of the glycated hemoglobins

A

HbA1c

263
Q

how is glycerinated haemoglobin formed?

A

non-enzymatic glycation of haemoglobin on exposure to glucose (predictable nature allows average blood glucose over prolonged time to be measured (6-8weeks) )

264
Q

what is the target HbA1c?

A

48 -58 mmol/mmol or 6.5%-7.5% (aim low for younger)

265
Q

what are factors affecting insulin absorption?

A 
Temperature
Injection site
Injection depth
Exercise
pen accuracy
leakage
266
Q

what can occur if too many injections to same site? what is advised?

A

lipohypertrophy

stop injecting there (as reduced absorption)

267
Q

insulin is a dangerous drug, what are some common errors made?

A

WRONG DOSE
INSULIN OMMISSION
WRONG INUSLIN TYPE

268
Q

how to avoid giving wrong insulin dose?

A 
Right patient
Right medicine
Right dose (use insulin syringe)
Right route
Right time

Additionally, insulin prescribing requires
Right documentation
Right monitoring
Right storage

269
Q

what is taken account of when prescribing insulin?

A 
Patient’s usual regimen and dose
Blood glucose monitoring
Ketone monitoring
Sepsis/acute illness
Steroid therapy
Age / lifestyle
if undergoing GA soon
270
Q

what must you not do even when patient is hypo?

A

Do not omit insulin if hypoglycaemic, treat hypo and administer insulin as usual (can reduce dose but don’t omit)

271
Q

when does alcohol affect insulin levels the most?

A

12-16 hours after (highest risk of hypo)

272
Q

what to do with insulin administration concerning exercise

A

reduce short acting dose by 20% + reduce long acting dose that night.

273
Q

what may be the future of insulin administration?

A

oral or inhaled insulin

274
Q

what to do if diabetic is sick?

A

follow sick day rules/guidelines

275
Q

when is IV insulin used?

A

Diabetic Ketoacidosis (DKA)

role in Hyperosmolar Hyperglycaemic State (HHS)

Acute illness

Fasting patients who are unable to tolerate oral intake

276
Q

IV insulin management/ monitoring key things to do?

A

Hourly blood glucose (BG) monitoring

Aim for BG 5 -12 mmol/L

Free of hypoglycaemia

Check ketones if BG > 12 mmol/L

Check U & E’s at least daily

Safe transition from IV to SC insulin

277
Q

what are the two types of pancreas transplant people can undergo?

A

Kidney-Pancreas Autotransplantation

Islet Autotransplantation

278
Q

when are transplants indicated?

A

Imminent or ESRD due to receive or with kidney transplant

Severe hypoglycemia/ metabolic complications

Incapacitating clinical or emotional problems

Endocrinology (7 decks)

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