T1DM Flashcards

Question

% adolescent w T1DM with hypertension

Answer 1

16% can predict future albuminuria

Answer 2

12yo start education in self care transition readiness assessmnets ID transition goals

Answer 3

q2years glycemic control freq/severity of hypoBG hypoBG awareness presence of micro- or macrovascular complications (retinopathy, neuropathy, nephropathy, amputation, CV dz) to ID if increased risk MVA

Answer 4

log of BG always have BG monitoring equipment and rapid carbs within reach measure BG prior to driving - should be >5 if <4 wait 40 min before driving measure BG q4h behind wheel or CGM wear medic alert bracelet Must refrain from driving immediately if have had severe hypoBG while driving and contact HCP

Answer 5

severe hypoBG while driving in past 12months more than 1 episode of severe hypoBG while away but not driving in: - 6m private driver - 12m commercial driver

Answer 6

Any condition that prolongs the life of the erythrocyte or is associated with decreased red cell turnover iron deficiency vitamin B-12 and folate deficiency anemias asplenia/splenomegaly uremia/chronic renal failure severe hyperTG severe hyperbili chronic alcohol anemia from blood loss pregnancy Vit E ingestion fructosamine

Answer 7

chronic renal failure splenomegaly rheumatoid arthritis use of erythropoietin, iron or B12 reticulocytosis chronic liver disease ingestion of aspirin, vit C or Vit E hemoglobinopathy hyperTG assay

Answer 8

1) macular edema = diffuse or focal vascular leakage at the macula (non-proliferative) 2) progressive accumulation of micro- vascular change that includes microaneurysms, intraretinal hemorrhage, vascular tortuosity and vascular malformation (together known as non-proliferative diabetic retinopathy) that ultimately leads to abnormal vessel growth on the optic disc or retina (proliferative diabetic retinopathy) 3) retinal capillary nonperfusion, a form of vascular closure detected on retinal angiography, which is recognized as a potential complication associated with diabetes that can cause blindness and currently has no treatment

Answer 9

Longer duration of DM High A1c Increased BP Dyslipidemia Anemia Pregnancy (with T1D) Proteinuria Severe retinopathy itself Modifiable: Glycemic control - ≤7% Blood pressure control Statin and fenofibrate – role in preventing development or progression is not established

Answer 10

- Laser therapy (i.e photocoagulation to retinal periphery when centre not involved) - Intraocular anti-VEGF (first line for centre-involving DME) - Vitrectomy – if complicated with non-clearing vitreous bleeding, persistent neovascularization (especially post laser or anti-VEGF) If visually disabled – refer for low-vision evaluation and rehab

Answer 11

T2D – at diagnosis and annually T1D - ≥15 y.o, ≥5 yrs diagnosis with poor metabolic control – annual Assessing loss of sensitivity to the 10g monofilament loss of sensitivity to vibration at the dorsum of the great toe (with tuning fork) pinprick or temperature ankle reflexes

Answer 12

Peripheral neuropathy (increase risk of foot ulcers and amputation) - loss of sensation in toes and feet, sharp shooting pains, burning, tingling, throbbing, numbness The involvement of large fibres may cause numbness, tingling and loss of protective sensation. Autonomic neuropathy: cardiac auto- nomic neuropathy [CAN]), gastrointestinal tract, genitourinary system, sexual function, pupillary responses and sweating mononeuropathies/focal neuropathies (median, ulnar, radial, common peroneal nerves), radiculoplexus neuropathy, cranial neuropathies - arrhythmias

Answer 13

elevated BG elevated TG high BMI smoking HTN

Answer 14

statin target LDL <2 or 50% reduction from baseline

Answer 15

BG >33 Bic >15 art pH >7.3 ven pH >7.25 Small ketonuria, absent to small ketonemia Osm >320 Obtundation, combativeness, seizures (50%)

Answer 16

increase pCOS2 above level the pt had been maintain may cause CSF pH to decrease => worsen cerebral edema

Answer 17

partially treated DKA starvation (anorexia or fasting low card/high fat diet SGLT2i

Answer 18

New: <2yo minority groups Low SES Known DM: Insulin omission Poor metabolic control or previous episodes of DKA Gastroenteritis with persistent vomiting and inability to maintain hydration Psychiatric d/o (esp eating d/o) Difficult or unstable family circumstances Peripubertal and adolescent girls Binge alcohol consumption Limit access to medical services

Answer 19

- Onset of headache after starting DKA treatment or worsening headache that was already present before starting treatment - Inappropriate slowing of heart rate - Recurrence of vomiting - Change in neurological status – restlessness, irritability, increased drowsiness, confusion, incontinence - Increase BP - Decrease O2 sat - Rapid increase Na conc 🡪 loss of urinary free water as manifestation of DI (from interruption of blood flow to pituitary gland due to cerebral herniation)

Answer 20

impending cerebral edema

Answer 21

- Restore circulating volume - Replace Na and extracellular and intracellular water deficits - `Improve glomerular filtration and enhance clearance of glucose and ketone from blood

Answer 22

1) Major loss is from the intracellular pool – because of transcellular shifts caused by hypertonicity, acidosis, and glycogenolysis & proteolysis due to insulin deficiency 2) K+ is lost from body from vomiting because of osmotic diuresis 3) Volume depletion causes secondary hyperaldosteronism -> urinary K+ excretion

Answer 23

hypophos: decreases ATP and 2,3-DPG -> metabolic encephalopathy, impaired myocardial contractility and resp failure (weakness of diaphragm), muscle dysfunction with proximal myopathy, dysphagia, and ileus Rhabdo if pre-existing severe PO4 depletion

Answer 24

One diagnostic criterion, two major criteria, or one major and two minor criteria have a sensitivity of 92% and a false positive rate of only 4% Diagnostic criteria - Abnormal motor or verbal response to pain - Decorticate or decerebrate posture - Cranial nerve palsy (especially III, IV, and VI) - Abnormal neurogenic respiratory pattern (eg, grunting, tachypnea, Cheyne-Stokes respiration, apneusis) Major criteria - Altered mentation, confusion, fluctuating level of consciousness - Sustained heart rate deceleration (decrease more than 20 beats per minute) not attributable to improved intravascular volume or sleep state - Age-inappropriate incontinence Minor criteria - Vomiting - Headache - Lethargy or not easily arousable - Diastolic blood pressure >90 mmHg - Age <5 years

Answer 25

Decreased fluids - maintain normal BP (avoid excess, also avoid hypotension) Head of bed 30 degrees, head midline Mannitol 0.5-1g/kg over 10-15min 3% saline - 2.5-5ml/kg over 15-30 min Do not delay tx for imaging!! Supportive therapy (O2, I&V, etc)

Answer 26

IVF bolus >/= 20ml/kg (assume 12-15% fluid deficit) Start insulin when BG no longer drops with IVF alone 0.025-0.05u/kg/h titrate dose to decreased BG 4-5.5/h add D2.5/5 if BG dropping too much want gradual decline in corrected Na and osmolality replace K as soon as K normal + normal renal fn replace Mg if severe hypoMg/hypoCa

Answer 27

- venous thrombosis (from rapid drop in BG/Osm + central venous Cath) - rhabdomyolysis (from AKI, severe hyperK, hypoCa, compartment syndrome) - malignant hyperthermia (reason unknown) - altered mental status (adults - not CE)

Answer 28

LGA SGA jaundice prematurity still birth hypoglycemia NICU cardiac (transient hypertrophic cardiomyopathy) skeletal malformations

Answer 29

- >35yo - from a high-risk group (African, Arab, Asian, Hispanic, Indigenous, or South Asian) - Corticosteroid medication - Obesity (BMI >/= 30 kg/m2) - Prediabetes - Gestational diabetes in a previous pregnancy - Given birth to a baby that weighed more than 4 kg - A parent, brother or sister with type 2 diabetes - Polycystic ovary syndrome or acanthosis nigricans

Answer 30

If high risk fo T2DM -> screen w HbA1c at first antenatal visit - If A1c ≥6.5% or FPG ≥7 – have diabetes in pregnancy - If negative – rescreen at 24-28 weeks All women screened at 24-28 weeks 50g GCT in nonfasting state - BG 1h later - BG ≥7.8 mmol/L at 1 h = positive screen and is an indication to proceed to the 75 g OGTT - BG ≥11.1 mmol/L = diagnostic of gestational diabetes and does not require a 75 g OGTT for confirmation If GCT screen positive -> 75 g OGTT dx of GDM if 1 of the following: - Fasting PG ≥5.3 mmol/L OR - 1 hour PG ≥10.6 mmol/L OR - 2 hours PG ≥9.0 mmol/L

Answer 31

MDI insulin Metformin is alternative but crosses the placenta - 40% will still need insulin Glyburide if decline insulin/metformin not tolerated

Answer 32

1) >/=2 Abs - euglycemia 2) >/=2 Abs - hyperglycemia 3) T1DM dx 4) Longstanding

Answer 33

HbA1c<5.7% Fasting BG <5.6 Oral GTT (2h BG) <7.8 Random BG <11

Answer 34

>/=6.5% >/= 7 >/= 11 >11 with symptoms

Answer 35

5.7-6.4% 5.6-6.9 7.8-11 ("glucose intolerance)

Answer 36

Earlier detection Exercise Highest safe insulin dose

Answer 37

Regular: - humulin R - Novolin Toronto - Entuzity

Answer 38

Aspart: - Novorapid - Fiasp Lispro - Humalog Glulisine: - Apidra

Answer 39

* Glargine ○ Basaglar ○ Lantus ○ Toujeo * Degludec ○ Tresiba * Detemir - Levemir

Answer 40

HyperBG -> hexokinase becomes saturated XS glucose in the cell -> glucose doesn’t get P’d -> gets converted to sorbitol sorbitol locks it in the cell because it cant cross the membrance -> it increases AGE on proteins

Answer 41

retinopathy

Answer 42

- lipohypertrophy - insulin edema

Answer 43

- Anti-GAD Ab - Anti-islet cell Ab - Anti-ZnT8 Ab - Anti- insulin - Anti-tyrosine phosphatase (IA2)

Answer 44

- Those with DR3/4-DQ8 or DR4/DR4 ○ with FH: 20% ○ w/o FH: 5%

Answer 45

Monozygotic twins risk: ~40% Risk to siblings, children: ~5%

Answer 46

Moderate amounts of alcohol can cause BGs to rise Excess alcohol can cause BGs to fall (competition in liver, glucagon release impeded) * Discuss relative alcohol and carb content of diff drinks * Recommend eating carb-containing foods before, during and after alcohol consumption * Discourage binge drinking (more than 4 drinks) * Alternate between alcohol and then a water * Avoid sugary alcoholic beverages * Check BG more frequently * Recommend eating a snack before bed * Set alarm to check BG during night to avoid noctural hypoBG * Recommend always wearing a medic alert bracelet * Discuss if friends would be able to recognize signs of hypoglycemia and intervene if necessary * Recommend not taking insulin for the CHO in drinks given that they the alcohol itself can lead to hypoglycemia * Glucagon may not work as well because of liver

Answer 47

* Check BG before, during and after exercise * Discuss possible delayed nocturnal hypoglycemia ○ Important to check BG overnight * Consider temporary basal rate during exercise to avoid hypoBG * In not reducing rate, recommend additional carbs before or during runs * Do not exercise if hyperBG and ketones >0.5 Give reduced insulin dose with carbs prior to exercise

Answer 48

pediatric endocrinologist or pediatrician with diabetes expertise dietician diabetes nurse educator social worker mental health professional

Answer 49

Causative and associated factors: Depression Eating disorders Lower socioeconomic status Lower family support Higher family conflict Additional factors during adolescence Physiologic insulin resistance Depression and other psychological issues Reduced adherence during a time of growing independence

Answer 50

New onset DM: Public awareness campaignes about S&S of DM Established DM: Education Behavioural intervention Family support Access to 24-hour telephone services or telemedicine for parents of children with diabetes

Answer 51

Diabetes distress Depression Anxiety Eating disorders Externalizing disorders

Answer 52

* Hygiene hypothesis – autoimmune hypersensitivity due to a lack of exposure to pathogens * Accelerator hypothesis - Increasingly obesogenic environment, which causes insulin resistance (which promotes the development of T1D in people with islet cell autoimmunity – high BG lead to stress and early destruction of beta cells) may account for the rise in incidence of T1D * Sunshine hypothesis – Less time spent outdoors (and covered up) leading to Vit D deficiency. Comes from the observation that countries closer to the equator have lower rates of T1D * Cows milk hypothesis – exposure to this early antigen (or lack of breastfeeding) disrupts the immune system and increases the risk of T1D i. v. Environmental triggers – pollution, viruses, toxins, immigrant populations etc. Genetics

Answer 53

Viruses Dietary factors (all small amount of risk) ○ Breast feeding/cows milk § BF- slightly decreases risk § Cows milk at young age - slightly increases risk Low Vitamin D, omega-3 fatty acids

Answer 54

1 Ab - ~14% 2 or more - 70-80%

Answer 55

Dawn phenomenon - overnight spike of counterregulatory hormones (usually ~2am): need to increase basal insulin around time of spike Simogyi effect - rebound hyperglycemia after a low

Answer 56

- regular physical activity -0.5% - CGM -1% - sensor-augmented pump -0.5%

Answer 57

- Recurrent severe hypoglycemia - Wide fluctuations in glucose levels regardless of HbA1c - Suboptimal diabetes control (i.e., HbA1c exceeds target of 7.0% or TIR is <70%) - Microvascular complications and/or risk factors for macrovascular complications - Targeted metabolic control but insulin regimen that compromises lifestyle - Young children and especially infants and neonates - Children and adolescents with pronounced dawn phenomenon - Children with needle phobia - Pregnant adolescents, ideally preconception - Ketosis prone individuals - Competitive athletes

Answer 58

In older children and adolescents expect a 50/50 split In children <7 years, basal insulin delivery may be 30%–35% of the TDD

Answer 59

- Celiac - Addison - Taking insulin to cause hypo - Incorrectly dosing insulin - Muchenhausen by poxy - ED - Meds - alcohol, ASA, oral hypoglycemic - severe illness affecting kidney or liver

Answer 60

- history of severe hypo - A1C <6% - long duration DM - adolescence - hypoBG unawareness - autonomic neuropathy - preschool children

Answer 61

- hypoK - hypoPhos - hypoCa - hypoMg - hypoBG - Hyperchloremic acidosis - Hypertryglyceridemia → acute pancreatitis - cerebral edema - VTE/PE - aspiration - cardiac arrhythmia - rhabdo - renal failure - ARDS

Answer 62

* 6-fold increase in risk of T2D in the child 1.8-fold increase in risk of T1D in the child

Answer 63

LGA/macrosomia -> shoulder dystocia -> brachial plexus injuries & perinatal asphyxia Preterm delivery Stillbirth Polycythemia TTN Hypoglycemia Hypocalcemia (hypopara) Hyperbilirubinemia Polycythemia MALFORMATIONS: Hypoplastic left colon, cardiac malformations (TGA, DORV, VSD, TA), hypertrophic cardiomyopathy Sacral agenesis/caudal dysplasia GI tract anomalies Neural tube defects

Answer 64

corticosteroids, catecholamines, glucagon, and GH

Answer 65

One diagnostic criterion, two major criteria, or one major and two minor criteria have a sensitivity of 92% and a false positive rate of only 4%. Diagnostic criteria ● Abnormal motor or verbal response to pain ● Decorticate or decerebrate posture ● Cranial nerve palsy (especially III, IV, and VI) ● Abnormal neurogenic respiratory pattern (eg, grunting, tachypnea, Cheyne-Stokes respiration, apneusis) Major criteria ● Altered mentation, confusion, fluctuating level of consciousness ● Sustained heart rate deceleration (decrease more than 20 beats per minute) not attributable to improved intravascular volume or sleep state ● Age-inappropriate incontinence Minor criteria ● Vomiting ● Headache ● Lethargy or not easily arousable ● Diastolic blood pressure >90 mm Hg ● Age <5 years

Answer 66

Benign postural proteinuria, diabetes related nephropathy, exercise induced proteinuria, febrile illness, UTI, acutely elevated glucose Decompensated CHF Menstruation Acute severe elevation in BG Acute severe elevation in BP

Answer 67

i) Optimizing glycemic control ii) Blood pressure control (<130/80) iii) Blocking RAAS – ACEi or ARB (independent of BP) iv) SGLT2 inhibitor (also has cardioprotection)

Answer 68

● Thick secretions plug pancreatic ducts causing a chronic pancreatitis like picture and beta cell damage ● Chronic steroid exposure ● High caloric and often carbohydrate intake ● Insulin resistance from chronic hyperglycemia causing down regulation of GLUT4 transporters ● CFTR channel on beta cells may play a role in insulin secretion ● Tube feeding

Answer 69

- 10 yo w OGTT (DO NOT DO A1C)

Answer 70

- CFRD - osteoporosis - short stature - male infertility - delayed puberty

Answer 71

Euglycemic Hyperinsulinemic Clamp Test 1. Primed continuous insulin infusion is administered to raise plasma insulin level to a predetermined physiological or pharmacological level 2. Plasma glucose concentration is measured q5min and variable GIR is administered to maintain the plasma glucose concentration constant at the fasting level 3. Given that plasma concentration of insulin is steady, the amount of exogenous glucose administered equals the amount of glucose utilized in response to the hyperinsulinemia and provides a direct measure of whole body sensitivity to insulin; can then predict Insulin

Answer 72

- Shift of K from intracellular to extracellular space in exchange with hydrogen ions that accumulate extracellularly in DKA → shifted K is lost by osmotic diuresis - Administration of insulin, leading to intracellular shift of K - Secondary hyperaldosteronism due to dehydration leading to excretion of K to hold on to Na/fluid for fluid repletion - low total K in body

Answer 73

- Patients may be more dehydrated so expect a larger fluid deficit, may need more boluses - Patients with HHS have larger whole body potassium / phosphate / magnesium deficits – monitor for these and replace as needed - Monitor CK regularly (every 2-3 hours) for rhabdoymyolysis - Use central venous catheters with caution, higher risk of thrombosis - Ketosis is usually minimal so early insulin administration is unnecessary. Initiate insulin when blood glucose is no longer falling with fluids alone. - may start with lower insulin concentration, 0.025-0.05 U/kg/hr

Answer 74

- Female - More severe disease - Pancreatic insufficiency

Answer 75

- no DKA - no macrovasc comp (do get microvasc)

Answer 76

- unexplained P&P - failure to gain or maintain wt - poor GV - delayed progression of puberty - unexplained decline in PFT MAY BE ASX

Answer 77

insulin - maybe just basal no oral antihyperglycemics

Answer 78

- Significant weight loss or weight gain - Preoccupation with food content, weight, or dieting - Purging behaviors – excessive exercise, laxative/diuretic use - Recurrent / frequent DKA - Distorted body image - Low mood - Worsened metabolic control, increased HbA1C - Missed or cancelled appointments - Changes in school attendanceE

Answer 79

- Female gender - Higher BMI - Low self esteem - History of depression - Family history of dieting or eating disorder

Answer 80

- emotional maturity, teens ability to sustain the daily Tasks of daily therapy - loss of parental supervision - reduced attendance to DM clinics - increased alcohol/substances - anxiety, depression - disordered eating - differing eating patterns as young adults become more independent - fear of hypo - knowlege gaps

Answer 81

- Urinary loss from osmotic diuresis - Reduced renal tubular reabsorption of phosphate - Shift of intracellular phosphate to the extracellular fluid compartment result of metabolic acidosis - Decreased intake (1 coming in, 1 shifting, 2 going out) Further decrease during tx: - Dilution from fluid replacement - Entry of phosphate into cells resulting from insulin treatment - Continuation of intravenous therapy without food consumption beyond 24 hours is a risk factor for clinically significant hypophosphatemia, although severe hypophosphatemia can also occur earlier in treatment *Main determinant is degree of acidosis

Answer 82

Normal eGFR or not rapidly declining No family history of nephropathy Lack of extreme proteinuria >6g/d Lack of persistent hematuria Diabetes > 5yrs Shouldn’t have signs or sx of another systemic disease other DM comp present too

Answer 83

reduced hypo

T1DM Flashcards

(113 cards)