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A Pathophysiology- BN607 > Case study: Ben (T2MD) > Flashcards

Case study: Ben (T2MD) Flashcards

1
Q

Who is Ben?

A

65-year-old plumbing warehouse manager.

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2
Q

When did Ben first start having symptoms, and what were they?

A

At 27. Was drinking (polydipsia) and peeing alot (polyuria).

Admitted to hospital with acute abdominal pain.

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3
Q

What did the drs discover when ben had his hospital admission at 27?

A

Found to have
- Glycosuria (more glucose than normal in the urine)
- Hyperglycemia
- Ketoacidosis (body produces too many ketones, increase blood acid)

Eventually diagnosed with acute pancreatitis and associated diabetes mellitus.

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4
Q

What are general risk factors for T2DM?

A
  • Obesity
  • Advanced age
  • Glucose intolerance
  • Pancreatitis or pancreatic cancer
  • Family hx of GI or DM
  • Gestational DM
  • Sedentary lifestyle
  • Certain infections
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5
Q

What is Bens family hx?

A
  • Father died of CA
  • Mums brothers died of MI
  • Ben’s brother had two MIs
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6
Q

Whats Bens social hx?

A
  • Drank heavy at the time. Beer.
  • Heavy smoker. 50 a day on wkds. 30 a day during the week. Gave up smoking at 32.
  • Moulder. Used to made taps. Then became incharge of the stores.

Was told if he had another drink it would kill him. Didn’t listen

  • Ben doesn’t drink now. Does not socialise as he used to. Happy having a diabetic lemonade.
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7
Q

Whats Bens weight hx?

A
  • Was overweight for his size. Was 138kgs, now down to 112kgs.
  • Talked about “yo yo diets”. Go mad for a week, then a couple weeks later back where you start and heavier.
  • Exercise a lot now. Can be doing up to 5-6 hours per day. This to try continue his weight loss.
  • Has one meal a day now. With a snack at maybe breakfast and tea time (biscuit or apple)
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8
Q

What were Bens risk factors for T2DM

A
  • Previous acute pancreatitis
  • Increasing weight/ obesity
  • Possibility excess alcohol consumption (High alc consumption increases risk of glucose intolerance, insulin resistance and therefore T2DM)
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9
Q

What is the main sign/ symptom of DM?

A

Hyperglycemia

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10
Q

What are additional signs and symptoms of diabetes?

A
  • Glycosuria (Sugar in urine)
  • Prolonged wound healing
  • Ketoacidosis
  • Recurrent infections
  • Fatigue
  • Weight loss
  • Polyuria (more urine than normal)
  • Polydipsia (excessive thirst)
  • Polyphagia (a feeling of extreme, insatiable hunger)
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11
Q

What signs and symptoms Ben had?

A
  • Hyperglycemia
  • Glycosuria
  • Polydipsia (Drinking a lot)
  • Polyuria
  • Ketoacidosis
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12
Q

What generally is diabetes explaiend as

A

Diabetes occurs when levels of blood glucose are too high due to insulin insufficiency.

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13
Q

What is T1DM?

A

Type 1 diabetes results when there is a total insulin deficiency, i.e. the pancreas does not produce an effective amount of insulin.

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14
Q

What is T2DM?

A

Type 2 diabetes is related to an insufficient amount of insulin production and/or insulin resistance.

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15
Q

What are the effects of excess glucose in the blood on the kidneys?

A

Excess amount of glucose being filtered at the kidneys.

Glucose transporters for reabsorption because saturated. Thus glucose remains in the filtrate/ urine - Leading to polyuria.

The excess water loss that occurs, leads to dehydration via increased plasma osmolarity, thus stimulating increased thirst (Polydipsia).

If fluid intake is not adequate, plasma osmolarity will be balanced by a fluid shift which can lead to cellular dysfunction.

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16
Q

Hyperglycemia can also lead to glycosylation. What is glycosylation?

A

The deposition of glucose on the basement membrane of blood vessels and neurons

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17
Q

What is the affect of Glycosylation?

A

Glycosylation affects the ability of substances to move into or out of the blood stream.

Causing tissue ischemia and poor inflammatory responses, poor wound healing and recurrent infections.

Glycosylation also affects action potential conduction.

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18
Q

What are complications of glycosylation?

A
  • Neuropathies (nerve damage)
  • Nephropathies (kidney disease)
  • Retinopathies (damnage to eyes)
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19
Q

How does the lack of glucose cause an increased reliance on lipid sources for energy?

A

The lack of glucose availability for cellular metabolism (for most body cells) means that there is increased reliance on lipid sources of energy.

Thus there is increased lipolysis and hyperlipidemia which can lead to cardiovascular complications such as atherosclerosis.

The increased use of fats for cellular metabolism also results in the production of ketone bodies, which are acidic and can lead to ketoacidosis, a significant complication of diabetes.

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20
Q

What are some complications of DM?

A
  • Retinopathy
  • Nephropathy
  • Autonomic neuropathy - Erectile dysfunction
  • Peripheral neuropathy, Peripheral sensorial loss
  • Gastrointestinal complications
  • Recurrent infections & poor wound healing
  • Foot complications/ Diabetic feet/ Foot ulceration
  • Gait alterations
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21
Q

What is Retinopathy?

A

Retinopathy is a common complication of diabetes. Blood vessel damage from a diabetic retinopathy can cause vision loss in two ways.

  • Macular edema
  • Proliferation retinopathy
22
Q

What is macular edema?

A

Fluid leaks into the part of the retina responsible for sharp, straight-ahead vision causing swelling and blurred vision

Can occur when blood vessels in the eye are damaged, resulting in leakage. Leads to swelling of the macula.

The swelling affects how the light rays stimulate the photoreceptors (mainly cones) within the macula.

Symptoms of macular oedema include blurred vision & washed out, or altered, color vision. Eventually this can lead to more severe vision loss and ultimately blindness.

23
Q

What is proliferation retinopathy

A

Fragile and abnormal new blood vessels form which easily break, leading to hemorrhages, scarring and retinal detachment

24
Q

What are the complications Ben has had with his vision from DM?

A

Basically blind in one eye.

Has macular problems.

25
Q

How can diabetes lead to vascular damage in the eye?

A

Hyperglycemia can lead to glycosylation of blood vessels, whereby glucose gets deposited in the basement membrane of capillaries.

Decreased effective gas, nutrient, and waste exchange. can lead to localised tissue damage, including microvascular damage.

Capillaries in the retina are particularly susceptible to this, as they are delicate network of blood vessels.

In ben’s case, the vascular damage has allowed leakage of fluid into the macua, causing macular oedema

26
Q

What is Nephropathy?

A

Nephropathy is the deterioration of kidney function.

Microvascular damage can also affect the glomeruli of the kidneys, leading to kidney disease.

In fact, diabetic nephropathy is a leading cause of renal failure. An individual with diabetes will have regular renal function tests & urinalysis.

27
Q

What aspects of Bens renal function laboratory results were out of scale?

A

Urea (mmol/L)

Creatinine (µmol/L)

eGFR (mL/min/1.73 m2)

28
Q

How does diabetes lead to autonomic neuropathy?

A

Hyperglycemia leads to glycosylation of neurons.

This disrupts normal action potential conduction, and when this occurs on neurons of the autonomic nervous system it can have an affect on a variety of systems.

29
Q

What are the gastrointestinal complications associated with autonomic neuropathy

A

Can include gastroparesis (Delayed gastric emptying), diarrhea and/or constipation.

30
Q

what gastrointestinal symptoms does Ben get?

A
  • Bloating. Going to bed ona full stomach made him bloat.

Gastroparesis is a condition that occurs when the stomach muscles don’t contract properly, causing food and liquid to remain in the stomach for too long. (Delayed gastric emptying). Fixed by reducing to one meal per day. No meals before bed or in the morning.

  • Diarrhea and constipation
31
Q

What was the effects on bens sex life?

A

Doesn’t get erections anymore.

Sensation starting going away around 18 years ago.

Did a test at the hospital- Took a viagra tablet. Worked but didn’t stop working for about four hours.

32
Q

What are the effects ben had on his blood pressure due to his autonomic neuropathy

A

Ben has a history of mild hypertension, for which he took medication at one stage.

In his later years he has had pretty good blood pressure control, but does experience some effects on blood pressure related to his autonomic neuropathy.

Stands up to quick can feel faint. Couple times have fallen due to this. Orthostatic hypotension. Normally sympathetic NS is activated to respond to this drop to quickly stabilize BP. With autonomic neuropathy, there is a distribution to the action potential output of sympathetic nerves involved with responding to the drop in BP, thus hypotension is not immediately corrected. Can cause dizziness, lightheadedness and fainting as reduced BP causes a reduced blood flow to the brain.

33
Q

What is peripheral neuropathy?

A

Peripheral neuropathy is similar to autonomic neuropathy in that glycosylation affects action potential conduction in neurons, however in this case, it is somatosensory neurons in the periphery (mostly the limbs) that are affected.

Peripheral neuropathy can have numerous effects beyond just sensory loss, including increased susceptibility to tissue damage, decreased wound healing and increased infection through a lack of sensory awareness. Such complications are, however, multi-factorial and may also relate to tissue ischemia & hypoxia and alterations to immune functioning related to vascular complications.

34
Q

What is Bens experience with peripheral neuropathy?

A
  • Feelings in legs (lower legs). Went to wash feet off with hose after working in garden and water wondering why the water wasn’t hotting his feet, but it was, just couldn’t feel it.
35
Q

What is Bens experience with poor wound healing and recurrent infections?

A

Had cellulitis. Got it every two months.

Cuts he would acquire and wouldn’t heal.

36
Q

What is Bens experience with foot issues?

A

Charcot’s joint in the foot. Lost of elasticity. Everytime he bends them feels like he’s breaking the skin. Feels tight. He can bend his foot and it moves, but he cant do it voluntarily.

Thought he had loose skin on toe. Went to pull it off but pulled the end of his toe off.

37
Q

What are Diabetic feet complications?

A
  • Ulcers
  • ischemia
  • Infections
  • Fallen arches
  • Edema
  • Charcot joints
  • Hammer toe
38
Q

What are the neuropathy effects on feet with diabetes?

A

If they have neuropathy there are three types that affect diabetes

  • Sensory (No feeling) loss of protective sensory, no feeling, injuries go undetected. Ulcer can deteriorate quickly.
  • Motor neuropathy: cause atrophy of muscle. Retraction of toes, hammer toes.
  • Autonomic neuropathy: Reduction or inability to sweat. Associated with charcot foot. Dryness of skin can lead to fissures.

Check that the pt does have peripheral vascular disease. Check they have a pulse. Symptoms of claudication/ ischemic foot.

39
Q

What are the foot pathologies ben experienced

A
  • sensorial loss
  • skin alterations
  • ischemia & ulceration
  • poor wound healing
  • Charcot joints
  • fallen arches
  • gait alterations

No sweating with feet. Dry.

40
Q

What is the normal range for blood glucose levels?

A

3 - 8 mmol/L

Fasting 3 - 5 mmol/L

41
Q

What is the ultimate goal of diabetes treatment?

A

The goal of diabetes treatment is to obtain euglycemia (normal BGLs) and correct any metabolic disorders

42
Q

What was Bens initial management?

A

After his initial presentation of acute pancreatitis with diabetes he was on high doses of insulin, but after 6 weeks he no longer exhibited signs of diabetes and his insulin treatment was ceased.

In subsequent years, his blood sugar levels began to rise again.

Was off insulin for probably 5 years

When got worse was on a tablet. Then insulin again.

43
Q

What management is bed on?

A

Placed on Metformin- an oral biguanide hypoglycemic agent that decreases gluconeogenesis and increases peripheral uptake/utilization of glucose.

Five years later put on insulin again.

Ben progressively made some changes to his diet, including decreasing alcohol intake, but for many years he struggled with weight control.

44
Q

What is bens insulin regime?

A

Humulin NPH (isophane insulin), a long acting insulin suspension using protamine.

He supplements this with the Humalog (insulin lispro) as necessary.

In the mornings take 28 units of insulin. In the evenings take 18 units. Humulin NPH.

Humalog taken as needed. If sugar is up in the morning has a chart f what doses to take.

45
Q

What is Humalog?

A

Rapid onset short acting insulin that can be taken shortly after meals to lower BGLs

46
Q

What are the advantages and disadvantages of using a chart to calculate insulin requirements?

A

Pros- Using a chart to calculate insulin is easy for people who have trouble figuring out how much insulin they need to take.

Con- Chart could be generic, and not specific to ben and how his body handles insulin.

47
Q

What is ben’s typical BGLs?

A

Normally in the mornings about 7-8 mmol/L

Dinner 4 mmol/L

Tea times 8-9-10 mmol/L

HbA1C- 7.3 %

48
Q

What is HbA1C and why is this a good indicator of glycemic control?

A

Glycosylated (glycated) hemoglobin.

Hemoglobin acculatees glucose over the lifetime of a RBC.

Glycosylated hemoglobin / HbA1C reflects the average plasma glucose concentration over the previous months.

Note that as of late 2011, measurement of HbA1c is reported in mmol/mol

49
Q

What were bens lab results for glycemic control?

A

Glucose (mmol/L)
2010: 6.4 mmol/L)
Ref range: 3.5 – 5.5

HbA1c (%)
2010: 7.3%
Ref range: 4.0 – 6.0

HbA1c (mmol/mol)
2010: 56 mmol/mol)
Ref range: 20 – 42

50
Q

What was bens DM managment?

A
  • Regular visits with his podiatrist to evaluate and treat his various foot pathologies. Check foot daily.
  • Medication
  • Glycemic control
  • Diet
  • Exercise; 100km bike a month
  • Weight loss
    Reduced his insulin requirement sufficiency and reduced his antihypertensive treatment
51
Q

What complications has Ben had due to his DM?

A
  • Autonomic neuropathy
  • Peripheral neuropathy
  • Recurrent cellulitis
  • Chargois joints
  • Postural hypotension
  • Impotence
  • Gastric symptoms
  • Retinal symptoms

A Pathophysiology- BN607 (28 decks)

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