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Pre final studying > Diabetes week > Flashcards

Diabetes week Flashcards

1
Q

What are the Causes of Secondary diabetes(4)

A 
Med or drug-related
exocrine pancreas related
endocrinopathy-related
infection 
other
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2
Q

Drugs that interfere with B cell release of insulin

A

cyclosporine
phenotoin
thiazides

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3
Q

Drugs that cause insulin resistance

A

glucocorticoids
niacin
antiviral phase inhibitor (HIV art therapy )

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4
Q

What drugs cause weight gain and beta-cell dysfunction (1)

A

antipsychotics

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5
Q

can blocking inhibitors of the autoimmune system cause diabetes
PD1 inhibitor
CILA-4 inhibitor

A

Yes

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6
Q

What are some causes of exocrine pancreatic related disease (genetic)

A

CF

hemochromatosis

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7
Q

What are some causes of exocrine pancreatic related disease (acquired) (5)

A 
Pancreatectomy
pancreatic cancer
infection 
trauma
pancreatitis
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8
Q

What are some endocrinopathy related diabetes(5)

A

1) acromegaly-> excessive growth hormone
2) Cushing’s syndrome
3) Cushings disease
4) topic crushing sign
5) pheochromocytoma

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9
Q

When do we do a T2D screen (3)

A

1) over 40 years old -> every 3 yrs
2) High risk individual (over a 33% change over 10 yrs)-> every 3 yrs
3) Very high risk and over 40 years old -> 6-12 months

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10
Q

Reasons to screen for T2D (7)

A

1) 40 or older
2) 1st degree relative with T2D
3) high-risk pop (not white)
4) History pre diabetes
5) hx of a macrosomic infant
6) Hx of GDM
7) if you see end organ damage

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11
Q

What are some vascular risk factors for T2D (6)

A

1) Smoker
2) HDL less than 1 in male fo less then 1.3 in female
3) triglycerdes are 1.7 or more
4) hypertension
5) overweight
6) abdominal obesity

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12
Q

Associated diseases with Diabetes (4)

A

PCOS (Polycystic ovarian syndrome)
HIV
OSA (Obstructive sleep apnea )
CF

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13
Q

What is CANRISK

A

Canadian diabetes risk assessment questions help assess risk of diabetes

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14
Q 
What are the diagnostic criteria for diabetes:
FPG
A1C
OGTT
Random PG
A

A1C over =6.5
FPG over =7.0
2hPG in a 75 g OGTT equal to or greater than 11.1 mol/L
RANDOM PG equal to or greater than 11.1 mol/L

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15
Q

draw chart for Sugars and A1c

A

see notes

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16
Q

What are the early manifestation fs of Hypoglycemia

A

1) tachycardia, palpitations
2) diaphoresis, anxiety
3) weakness hunger and nausea

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17
Q

What are the long term manifestations of hyperglycemia

A

1) coma, confusions hallucinations seiers

hypothermia

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18
Q

What are the early manifestations of hyperglycemia

A

1) Polydipsia, polyuria
2) altered vision
3) decrease wieght mild dehydration

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19
Q

What are the stages of progression of Diabetic nephropathy

A

1) Hyperfiltration with increased GFR
2) silent
3) Microalbumnia->1st sign of diabetic nephropathy (urine acr)
4) macro albuminuria

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20
Q

Screening of nephropathy

A

1) creatine and GFR-> 1 time a year
increase to 3-6moths is abnormal
2) Spot ACR once a year -> if positive need to do a lot

T1D -> start within 5 yrs of diagnosis
T2D -> Right away

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21
Q

What are the 2 types of Diabetic retinopathy ?

A

1) non-proliferative microvascular changes
thicking of the basement membrane,per cycle loss
altered vascular tone proliferation f not hial cells
2) Proliferative DR
severe hypoxia
new vessles

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22
Q

Classes of Retinopathy

A

1) Diabetic retinopathy

2) diabetic macular edema

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23
Q

Diagnosis of retinopathy

A 
fundoscopy 
- cotton wool spots
hard exudates
neovascualrition 
microanuerism

Optical coherence tomography for diabetic macular edema

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24
Q

What is Optical coherence tomography

A

Optical coherence tomography for diabetic macular edema thing in eye see an increase edema

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25
Q

retinopathy treatment

A

1) anti vEGF antibodies
2) photocoagulation for DME
3) Vitrectomy (removal of citrus humour)

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26
Q

Diabetic neuropathy types

A

1) distal symmetric polyneuropathy (stocking-glove)
2) radiculopathy plexopathy
3) mononeuropathy
4) autonomic neuropathy

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27
Q

What kind of test can you do for Diabetic neuropathy

A

monofiliments 10 g

tuning fork

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28
Q

treatment Diabetic neuropathy

A

gabapetniods
snri antidepressants
tireyelic antidepresesent

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29
Q

What are the ABCDES of preventing the microvascular

A 
A- keep A1C <= 7%
B-Blood pressure below 130/80 mmHg
C- Cholesterol keep LDL below 2 mmol/L
D- Drugs to protect heart and kidneys 
E- Eat healthily and exercise
S- Stop smoking
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30
Q

What are the macrovascular complication of diabetes (3)

A

1) Cardiovascualr
2) Cerebrovascualr
3) Periferla vasculr

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31
Q

what is the goal of prevention of T2D goals for a prediabetic- (3)

A

1) Delay the onset of T2D
2) prevent microvascular complications
3) preserve your b cells

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32
Q

Prediabetes recommendations

A

1) moderate weight loss
2) 150 mins/week
3) mediterian diet
4) metformin

33
Q

Effects of epinephrine

A 
promote glucose uptake
increase glycogenolysis
and gluconeogenesis
promotes glycolysis 
inhibits insulin secretion 
promotes lipolysis
helps realize GLUT4 without insulin
stimulates glucagon
34
Q

What are some methods of measuring glucose (5)

A

2) rt CGM -> Dexcom gives real-time on the phone
3)Capillary glucose montior
4) bionic pancreas
5) urine test

35
Q

A1C targets Adults with T2D to reduce the risk of CKD and retionpathy if at low risk of hypoglycemia

A

below 6.5

36
Q

A1C targets Adults with T2D and T1D

A

equal to 7 or less

37
Q

end of life A1C targets

A

7.1-8.5 we don’t really care

38
Q

Diagnositc critrea for pre diabets

A

A1C 6.0-6.4

FPG 6.1-6.9

39
Q

Diagnostic critirea for metabolic disorder

A

1) Waist circumfernce -> M:102 cm F:88 cm
2) Triglycrides >=1.7
3) HDL below M1.0 F1.3
4) hypertension
5) elevated FPG >=5.6

40
Q

What test do you do for Diabetie neropapthy

A

tuning fork and microfiliment

41
Q

When do we do ECG for diabetes

A

every 3-5 yrs

42
Q

What is Charcot foot

A

Broken/deformed diabeteic foot for diabetes patient

43
Q

Red foot Ddx

A

1) Cellulits/osteomyletis
2) charchot arthopy
3) inflammatoru gouty artihits
4) DVT
5) inflamitory arthitius

44
Q

Beta cells what do they seceerte and precentage

A

Insulin

80%

45
Q

alpha cells what do they seceerte and precentage

A

glucagon

15-20%

46
Q

Delta cells what do they seceerte and precentage

A

Somatostatin

3-10%

47
Q

What does somatostatin do?

A

Inhibits insulin and glucagon

48
Q

PP cells what do they seceerte and precentage

A

pancretic poly peptide

3-5%

49
Q

What is the parasympathetic innervation of the islet cells and what is the neurotransmitter

A

vagus
ach
increase insulin release

50
Q

What is the sympathetic innervation of the islet cells and what is the neurotransmitter

A

postganglionic fibres of the celiac ganglion

noreepinephrene

51
Q

What stimulates insulin release

A 
Hormones
1) GLP-1
2) GIP
3) Ach
4) Glucagon
nutrients 
1) Glucose
2) Arg and lys
3) FFA
52
Q

What inhibits insulin release

A

Noreepinephrine/epinephrine
somatostatin
tomuch sugar or ffa

Glucocorticoids and growthhormone

53
Q

How is insulin released stimulated pathway

A

glucose flows into cell- increase in ATP/ADP
inhibits k plus channel-> Ca influx-> depolrizaiton
Insulin release

54
Q

Roles of insulin (3)

A

Promotes energy storage anabolic
target muscule fat and liver
large role in growth and developemnt

55
Q

How does insulin stim glucose uptake

A

hits tyrosine kinase receptor GlUT4 release

56
Q

What stimulates glucagon release

A 
Nutrients
1) Arg ala
2) lack of glucose
Hormones
1) CCK
2) GIP
3) Noreephrene, ach , epinerphreine
57
Q

What inhibits glucagon release

A

Somatostatin
insulin
GLP-1

58
Q

What are three features of DKA

A

1) Hyperglycemia
2) ketones
3) acidosis ph less then 7.35, aniongap

59
Q

What are the 6 sings and symptoms we would see with DKA

A

1) prodrome of polydipsia,weakness,polyureia,nausea vomiting abdo pain
2) Volume dpletion
3) kussmalt breathing
4) Acetone breath
5) Myalgia
6) normal temp or hypothermia

60
Q

In DKA will we see and anion gap and waht is a normal anion gap

A

yes

Normal-10-14

61
Q

What are 4 precipitating causes of DKA

A

1) acute illness
2) New onset of diabetes
3) Insulin under dose
4) Drugs ->cocaine,

62
Q

6 steps to manage DKA

A

1) Volume repletion
2) Insulin bolus to stop acidosis
3) K plus repletion
4) decrease plasma glucose with insuiln
5) Fix percitpating cause
6) monitor everything

63
Q

What is there a risk of in pediatirc DKA

A

Cerebreal edema

64
Q

Signs and symptoms of Cerebreal edema (6)

A

1) decreased mental statues
2) age inapportpe incontinace
3) focal neurological defects
4) headaches
5) cushings triade
6) hypoxemia

65
Q

What are the 3 features of cushings triad

A

1) hypertension
2) bradycardia
3) irregular resp

66
Q

Managment of Cerebreal edema (4)

A

1) Hypertonic saline or manitol
2) elevate head
3) decrease iv fluid by 1/3
4) might need intubation

67
Q

Are you hyponatrimec or hypernatrimeic in DKA

A

hyponatrimic

68
Q

Potasium loss in DKA

A

can be either hypokalemic or hyperkalemics
but overal in a k plus depleted state

increased rasas and osmotic dirises of k+

Insulin defiencty leads to less k plus uptake in cells k plus hplus exchange in acidosis
also decrease volume so it increase

69
Q

Anion gap equation

A

Na-cl–HCO3

70
Q

what are features hyperglycemic hyperosmolar state? (3)

A

1) severe hyperglycemia
2) hyperosmolity
3) volumdelpeted

71
Q

Clincal features of HHS

A

Old 60plus
poor fludi intake
prodonre polydyipsia and polyuria
weakness confuisin

72
Q

What can cause HHS other then being old

A

1) acute illnesss

2) drugs

73
Q

How can u monitro Blood glucose

A

Capillary blood glucose
interminttenly scanned flash coninue saccaned glucose
continues glusoce monitor =realtime glucose monitor-> dexcoem on phone

74
Q

Moleculre mech of glucose toxity

A

1) polyol aldose reducates pathway acivation
2) ADvanced glycosltyion end product ACE formation
3) Protien kinace C activation
4) hexosamine pathway

75
Q

polyol aldose reducates pathway acivation

A

sugar overwhelms aldose reducates and ROS builds up leads to cell damage

76
Q

Advanced glycosltyion end product ACE formation

A

increase glucos eleads to increase glycoslytino bad signaling

77
Q

Protien kinace C activation

A

PKC is an intracellular messenger increase glucosse increases PKC cause leackage o blood vessles and clots increase vasoconstriction

78
Q

hexosamine pathway

A

alternate oathway for glucose alters mrna expresion and protien production

Pre final studying (8 decks)

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