Diabetes week Flashcards
What are the Causes of Secondary diabetes(4)
Med or drug-related exocrine pancreas related endocrinopathy-related infection other
Drugs that interfere with B cell release of insulin
cyclosporine
phenotoin
thiazides
Drugs that cause insulin resistance
glucocorticoids
niacin
antiviral phase inhibitor (HIV art therapy )
What drugs cause weight gain and beta-cell dysfunction (1)
antipsychotics
can blocking inhibitors of the autoimmune system cause diabetes
PD1 inhibitor
CILA-4 inhibitor
Yes
What are some causes of exocrine pancreatic related disease (genetic)
CF
hemochromatosis
What are some causes of exocrine pancreatic related disease (acquired) (5)
Pancreatectomy pancreatic cancer infection trauma pancreatitis
What are some endocrinopathy related diabetes(5)
1) acromegaly-> excessive growth hormone
2) Cushing’s syndrome
3) Cushings disease
4) topic crushing sign
5) pheochromocytoma
When do we do a T2D screen (3)
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
Reasons to screen for T2D (7)
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
What are some vascular risk factors for T2D (6)
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
Associated diseases with Diabetes (4)
PCOS (Polycystic ovarian syndrome)
HIV
OSA (Obstructive sleep apnea )
CF
What is CANRISK
Canadian diabetes risk assessment questions help assess risk of diabetes
What are the diagnostic criteria for diabetes: FPG A1C OGTT Random PG
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
draw chart for Sugars and A1c
see notes
What are the early manifestation fs of Hypoglycemia
1) tachycardia, palpitations
2) diaphoresis, anxiety
3) weakness hunger and nausea
What are the long term manifestations of hyperglycemia
1) coma, confusions hallucinations seiers
hypothermia
What are the early manifestations of hyperglycemia
1) Polydipsia, polyuria
2) altered vision
3) decrease wieght mild dehydration
What are the stages of progression of Diabetic nephropathy
1) Hyperfiltration with increased GFR
2) silent
3) Microalbumnia->1st sign of diabetic nephropathy (urine acr)
4) macro albuminuria
Screening of nephropathy
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
What are the 2 types of Diabetic retinopathy ?
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
Classes of Retinopathy
1) Diabetic retinopathy
2) diabetic macular edema
Diagnosis of retinopathy
fundoscopy - cotton wool spots hard exudates neovascualrition microanuerism
Optical coherence tomography for diabetic macular edema
What is Optical coherence tomography
Optical coherence tomography for diabetic macular edema thing in eye see an increase edema
retinopathy treatment
1) anti vEGF antibodies
2) photocoagulation for DME
3) Vitrectomy (removal of citrus humour)
Diabetic neuropathy types
1) distal symmetric polyneuropathy (stocking-glove)
2) radiculopathy plexopathy
3) mononeuropathy
4) autonomic neuropathy
What kind of test can you do for Diabetic neuropathy
monofiliments 10 g
tuning fork
treatment Diabetic neuropathy
gabapetniods
snri antidepressants
tireyelic antidepresesent
What are the ABCDES of preventing the microvascular
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
What are the macrovascular complication of diabetes (3)
1) Cardiovascualr
2) Cerebrovascualr
3) Periferla vasculr
what is the goal of prevention of T2D goals for a prediabetic- (3)
1) Delay the onset of T2D
2) prevent microvascular complications
3) preserve your b cells
Prediabetes recommendations
1) moderate weight loss
2) 150 mins/week
3) mediterian diet
4) metformin
Effects of epinephrine
promote glucose uptake increase glycogenolysis and gluconeogenesis promotes glycolysis inhibits insulin secretion promotes lipolysis helps realize GLUT4 without insulin stimulates glucagon
What are some methods of measuring glucose (5)
2) rt CGM -> Dexcom gives real-time on the phone
3)Capillary glucose montior
4) bionic pancreas
5) urine test
A1C targets Adults with T2D to reduce the risk of CKD and retionpathy if at low risk of hypoglycemia
below 6.5
A1C targets Adults with T2D and T1D
equal to 7 or less
end of life A1C targets
7.1-8.5 we don’t really care
Diagnositc critrea for pre diabets
A1C 6.0-6.4
FPG 6.1-6.9
Diagnostic critirea for metabolic disorder
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
What test do you do for Diabetie neropapthy
tuning fork and microfiliment
When do we do ECG for diabetes
every 3-5 yrs
What is Charcot foot
Broken/deformed diabeteic foot for diabetes patient
Red foot Ddx
1) Cellulits/osteomyletis
2) charchot arthopy
3) inflammatoru gouty artihits
4) DVT
5) inflamitory arthitius
Beta cells what do they seceerte and precentage
Insulin
80%
alpha cells what do they seceerte and precentage
glucagon
15-20%
Delta cells what do they seceerte and precentage
Somatostatin
3-10%
What does somatostatin do?
Inhibits insulin and glucagon
PP cells what do they seceerte and precentage
pancretic poly peptide
3-5%
What is the parasympathetic innervation of the islet cells and what is the neurotransmitter
vagus
ach
increase insulin release
What is the sympathetic innervation of the islet cells and what is the neurotransmitter
postganglionic fibres of the celiac ganglion
noreepinephrene
What stimulates insulin release
Hormones 1) GLP-1 2) GIP 3) Ach 4) Glucagon nutrients 1) Glucose 2) Arg and lys 3) FFA
What inhibits insulin release
Noreepinephrine/epinephrine
somatostatin
tomuch sugar or ffa
Glucocorticoids and growthhormone
How is insulin released stimulated pathway
glucose flows into cell- increase in ATP/ADP
inhibits k plus channel-> Ca influx-> depolrizaiton
Insulin release
Roles of insulin (3)
Promotes energy storage anabolic
target muscule fat and liver
large role in growth and developemnt
How does insulin stim glucose uptake
hits tyrosine kinase receptor GlUT4 release
What stimulates glucagon release
Nutrients 1) Arg ala 2) lack of glucose Hormones 1) CCK 2) GIP 3) Noreephrene, ach , epinerphreine
What inhibits glucagon release
Somatostatin
insulin
GLP-1
What are three features of DKA
1) Hyperglycemia
2) ketones
3) acidosis ph less then 7.35, aniongap
What are the 6 sings and symptoms we would see with DKA
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
In DKA will we see and anion gap and waht is a normal anion gap
yes
Normal-10-14
What are 4 precipitating causes of DKA
1) acute illness
2) New onset of diabetes
3) Insulin under dose
4) Drugs ->cocaine,
6 steps to manage DKA
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
What is there a risk of in pediatirc DKA
Cerebreal edema
Signs and symptoms of Cerebreal edema (6)
1) decreased mental statues
2) age inapportpe incontinace
3) focal neurological defects
4) headaches
5) cushings triade
6) hypoxemia
What are the 3 features of cushings triad
1) hypertension
2) bradycardia
3) irregular resp
Managment of Cerebreal edema (4)
1) Hypertonic saline or manitol
2) elevate head
3) decrease iv fluid by 1/3
4) might need intubation
Are you hyponatrimec or hypernatrimeic in DKA
hyponatrimic
Potasium loss in DKA
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
Anion gap equation
Na-cl–HCO3
what are features hyperglycemic hyperosmolar state? (3)
1) severe hyperglycemia
2) hyperosmolity
3) volumdelpeted
Clincal features of HHS
Old 60plus
poor fludi intake
prodonre polydyipsia and polyuria
weakness confuisin
What can cause HHS other then being old
1) acute illnesss
2) drugs
How can u monitro Blood glucose
Capillary blood glucose
interminttenly scanned flash coninue saccaned glucose
continues glusoce monitor =realtime glucose monitor-> dexcoem on phone
Moleculre mech of glucose toxity
1) polyol aldose reducates pathway acivation
2) ADvanced glycosltyion end product ACE formation
3) Protien kinace C activation
4) hexosamine pathway
polyol aldose reducates pathway acivation
sugar overwhelms aldose reducates and ROS builds up leads to cell damage
Advanced glycosltyion end product ACE formation
increase glucos eleads to increase glycoslytino bad signaling
Protien kinace C activation
PKC is an intracellular messenger increase glucosse increases PKC cause leackage o blood vessles and clots increase vasoconstriction
hexosamine pathway
alternate oathway for glucose alters mrna expresion and protien production
