Diabetes Flashcards

1
Q

Give a brief history of diabetes

A

Clinical features similar to diabetes mellitus described more than 3500yrs ago by ancient Egyptians .
•Indians/Arabs – had also described it , eg Avicenna , an arabian physician described among other things the complications – peripheral neuropathy, gangrene and erectile dysfunction
•Araetus of Cappodocia( 81-133AD)- named it Diabetes- TO SIPHON(named so cuz the people w Diabetes were urinating bunch as in they were losing fluid
•Thomas Willis – Britain ( 1675)- added Mellitus which means Sweet
Macleod and Collin isolated insulin

Insipidus means tasteless

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

What is diabetes
Explain how it occurs

A

Diabetes mellitus is heterogenous group of metabolic diseases characterized by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, or both.

Or it is a complex chronic metabolic disease and is associated with relative or absolute impaired insulin secretion
Along with varying degrees of peripheral resistance to insulin

So in a normal person, the pancreas produces jnsuoin and this insulin binds to insulin receptors on the cell to allow glucose to enter into the cell
In type 1 diabetes, the pancreas doesn’t produce the insulin in the first place so it can’t bind to the insulin receptors hence it stays outside in the blood.
In type 2, the pancreas produces but the cell doesn’t respond to the insulin produced properly so the insulin is there alright but the glucose is still in the blood.

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

Name five types of diabetes
How does phaeo cause high bp and dm
How do steroids cause high glucose
How does Cushing syndrome cause dm

A

ADA classification:

Type 1
•Type 2
•Monogenic diabetes
•LADA
•DM associated with endocrinopathies- acromegaly, cushings, pheo( catecholamines produced too much. Leads to high bp and One of the classical symptoms of pheochromocytoma crisis is hyperglycemia [1] that might be caused by increased insulin resistance in peripheral tissues and impaired insulin secretion [2]. ) ,glucagonoma
•Genetic syndrome- downs , turners syndrome, klienefelters syndrome
•Drug induced eg- steroids or glucocorticoids , post transplant medication, iv pentamidine
•Dx of exocrine pancreas- ca pancreas, pancreatitis, trauma, pancreatectomy, cystic fibrosis
•GESTATIONAL DM

Phaeo:

Catecholamines and a number of other hormones released during stress states contribute to the development of hyperglycemia by directly stimulating glucose production and interfering with tissue disposal of glucose.

Epinephrine causes a prompt increase in blood glucose concentration in the postabsorptive state. This effect is mediated by a transient increase in hepatic glucose production and an inhibition of glucose disposal by insulin-dependent tissues.

Norepinephrine (NE) and epinephrine (Epi) help maintain normal blood glucose levels by stimulating glucagon release(Insulin controls whether sugar is used as energy or stored as glycogen. Glucagon signals cells to convert glycogen back into sugar. Glucagon is a glucoregulatory peptide hormone that counteracts the actions of insulin by stimulating hepatic glucose production and thereby increases blood glucose levels.) , glycogenolysis, and food consumption, and by inhibiting insulin release.

Steroids:

How do steroids induce or bring on diabetes? Normally, the liver reduces the amount of glucose it releases in response to insulin. Steroids make the liver less sensitive to insulin so it carries on releasing glucose even if the pancreas is releasing insulin.

Steroids can increase your blood sugar level in different ways. They can:

cause the liver to release more glucose
stop glucose being absorbed from the blood by the muscle and fat cells
reduce the body’s sensitivity to insulin.
All these things can mean too much glucose stays in your blood. This can lead to diabetes.

Cushing’s syndrome is a condition in which can occur if you have high levels of the stress hormone, cortisol, in your blood. Cortisol increases our blood pressure and blood glucose levels and diabetes is one complication which can result from untreated Cushing’s syndrome.

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

State some characteristics of type 1 DM,which people does it usually occur in,what does it usually present w,state three antibodies that are identified in the blood of someone w type 1 DM

A

About 5 percent of all diabetics
•X’RISED BY cell mediated AUTOIMMUNE DESTRUCTION OF THE B CELLS
•USUALLY OCCURS IN CHILDREN
•HOWEVER ADULTS CAN ALSO HAVE TYPE 1- LADA
•USUALLY PRESENTS WITH DKA
•AUTOANTIBODIES IDENTIFIED INCLUDE- ICA, GAD65, IA-2A,

Type 1 is insulin dependent
Beta cells produce insulin so if it’s destroyed by antibodies there won’t be enough insulin

Type 1 continued
•Exact cause not known
•Associated with HLA DR/DQ
•MAY BE TRIGGERED BY VIRAL INFECTION

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

What is LADA and state the full meaning

A

Not a type of DM on it own
•Category to identify adults with Type 1 diabetes
•Associated with autoantibodies

Latent autoimmune diabetes of adulthood (LADA)

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

Explain type 2 diabetes

A

About 90-94% of all diabetics
•X’rised by insulin insensitivity and relative insulin deficiency
•Usually occurs in adults
•However due to childhood obesity, incidence increasing in children
•Usually associated with complications at the time of diagnosis

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

Name the characteristics of ominus octet

A

INSULIN RESISTACE IN THE MUSCLES- >POOR GLU UPTAKE
•INSULIN RESISTANCE IN THE LIVE-> OVERPRODUCTION OF GLU
•B CELL FAILURE
•INCREASE LIPOLYSIS
•INCREASE GLUCOSE ABSORPTION BY THE KIDNEYS
•INCRETIN DEFICIENCY/RESISTANCE
•INSULIN RESISTANCE IN THE BRAIN
•ALPHA CELL HYPERPLASIA> HYPERGLUCAGONOMA

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

State the differences between type 1 and type 2 diabetes

A

Type 1 the onset is sudden
Type 2 onset is gradual

Type 1 occurs at any age (mostly young people)
Type 2 occurs mostly in adults

Type One occurs in thin or normal people
Type 2 occurs in obese people

Ketoacidosis is common in type 1
It’s rare in type 2

Autoantibodies is usually present in type 1
It’s absent in type 2

Endogenous insulin is low or absent in type 1
It’s normal,decreased or increased in type 2

50percent concordance in identical twins in type 1
90 percent concordance in identical twins in type 2

Type 1 is less prevalent
Type 2 is more prevalent
90percent concordance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

State the differences between LADA and type 2 diabetes

A

LADA-LOWER BMI
Type 2-INCREASED BMI

LADA-USUALLY NOT ASSOCIATED WITH Type 2-METABOLIC SYNDROME
ASSOCIATED WITH METABOLIC SYNDROME

LADA-NOT ASSOCIATED WITH POSITIVE FAMILY HISTORY
Type 2-POSITIVE FAMILY HISTORY

LADA-AGE OF ONSET 30-50YRS
Type 2-AGE OF ONSET >50 YRS

LADA-C- PEPTIC LEVELS ARE LOW
Type2-C- PEPTIDE LEVELS NORMAL OR HIGH

LADA-AUTOANTIBODIES PRESENT
Type2-AUTOANTIBODIES ABSENT

LADA-ASSOCIATED WITH SPECIFIC HLA –HLA DQB1
Type 2-GENETICS IS COMPLEX

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

State the two types under monogenic diabetes Mellitus
What is monogenic dm
What is MODY

A

1.Neonatal DM-What Is Neonatal Diabetes? Neonatal diabetes mellitus is a rare form of diabetes that occurs within the first 6 months of life. Our bodies need insulin to help our cells make energy. Infants with this condition do not produce enough insulin, which increases blood glucose levels.

2.MODY

Monogenic diabetes is a rare condition resulting from mutations (changes) in a single gene. In contrast, the most common types of diabetes—type 1 and type 2—are caused by multiple genes (and in type 2 diabetes, lifestyle factors such as obesity).

MODY stands for “Maturity-onset diabetes of the young” and was given that name in the past because it acted more like adult type of diabetes (Type 2 Diabetes) but was found in young people. MODY limits the body’s ability to produce insulin, but is different than the juvenile type of diabetes (Type 1 Diabetes).

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

Name four Characteristics of MODY

A

USUALLY OCCUR IN YOUNG INDIVIDUALS/ CHILDREN
•AUTOSOMAL INHERETANCE PATTERN
•MORE THAN 8 GENETIC MUTATIONS IDENTIFIED
•COMMON TYPES- HNF4B, GCK, HNF-1A ETC
•SOME OF THESE INDIVIDUAL ARE SENSITIVE TO SULPHANYLUREAS

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

Name the complications of DM

A

•TYPICALLY GROUPED INTO
•MICROVASCULAR COMPLICATIONS (small vessels)eg- nephropathy, retinopathy, NEUROPATHY
•MACROVACULAR COMPLICATIONS eg peripheral artery dx, stroke, myocardial infarction
•RECURRENT INFECTIONS- UTIs , SKIN INFECTIONS( FURUNCULOSIS, CELLULITIS ,FORNIER’S GANGRENE ETC)
If person is getting boils by heart check for diabetes

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

Hyperglycemia isn’t as dangerous as hypoglycemia but hypo is an emergency

True or false

A

True

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

Cortisol pushes sugar into the blood while insulin pushes sugar to the tissues true or false

A

True

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

CAUSE OF BLINDNESS IN ADULTS ( 20-70YRS)
•LEADING CAUSE OF NON TRAUMATIC LOWER EXTREMITY AMPUTATION
•ESRD ABOUT 20-30%

In DM true or false

A

True

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

What are the typical symptoms of insulin deficiency

A

Typical symptoms of insulin deficiency- polyuria, polydipsia, polyphagia, weight loss
•Take history of possible complications

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

How is DM diagnosed

What is the normal ,prediabetic and diabetic values or ranges for RBS,FBS,HbA1C,OGTT

A

FBS RBS use two or more values to determine if a person has diabetes

If the person has the classical signs of diabetes you can accept a high value of FBS or RBS checked once

FBS
3.9-5.5-normal
≥5.6-<7-prediabetes
>7-diabetes Mellitus

RBS
4-7.8-normal
≥7.8-<11-prediabetes
>11-diabetes Mellitus

OGTT
3.9-5.5-normal

≥7.8-<11-prediabetes

> 11-DM

HBA1C
<5.6-normal
≥5.6-<6.4-prediabetes
>6.5-DM

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

Name ten tests that are done in DM

A
FBC
•BUE/CR
•LFT
RFT
•HBA1C
•UACR
•LIPIDS
•URINE R/E
  • TEST FOR AUTOANTIBODIES-
  • ICA- ISLET CELL CYTOPLASMIC ANTIBODIES
  • GAD- GLUTAMIC ACID DECARBOXYLASE AUTOANTIBODIES
  • INSULIN ANTIBODIES
  • IA-2A- INSULINOMA ASSOCIATED-2 AUTOANTIBODIES

C PEPTIDE LEVELS
•GENETIC TESTS FOR SPECIFIC MUTATIONS

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

How is DM managed,pharmacological,non pharmacological

A
MULTIDICIPLINARY-
•Dietician
•Physical Therapist
•Nurses
•Clinicians
•Ophthalmologists
•Podiatrists

DRUGS or pharmacological
•ORAL HYPOGLYCEMIA DRUGS
•ORAL HYPOGLYCEMIC AGENTS- BIGUANIDES, TZD, SU, MEGLITINIDE, DPP4 INHIBITORS, GLP 1 AGONISTS, SGLT 2 ANTAGONISTS
•INSULIN-

  • CONTROL OF HYPERTENSION
  • CONTROL OF LIPID LEVELS
  • SCREEN FOR EARLY ONSET OF COMPLICATIONS AND INSTITUTE APPROPRIATE CARE
FBS/GLUCOSE PROFILE
•3-4 MONTHLY HBA1C
•YEARLY LIPIDS
•YEARLY UACR
•YEARLY OPHTHOMOLOGIST REVIEW
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

It’s better to catch diabetes early at the pre diabetic stage true or false

A

True

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

Name some complications of diabetes Mellitus

A

Acute- hypoglycemia, hyperglycemia, hhs, dka

•Chronic- microvascular and macrovascular

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

What blood glucose value is considered as hypoglycemia

State four causes of hypo

And six symptoms of hypo

A

Blood glucose < 3.1mmol/l
•Mismatch of carbohydrate availability and hypoglycemic agents

Causes
•Overdosage of insulin or hypoglycemic agents
•Undereating
•Unplanned exercise
•Skipping or omitting meals
•Stress / overexertion

Symptoms

Sweating
•Lightheadedness
•Tremors
•Palpitations
•Irritability/ behavioural changes/confusion
•Yawning
•Anxiety
•Seizures
•Comapermanent brain damage death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is mild hypoglycemia managed

A
Give simple sugars p.o.(15gm of rapid acting sugar)
Examples:
-8oz of fruit juice
8oz of skim milk
3glucose tablets
3-4oz of regular soft drinks
3-4pieces of hard candy
1tbsp of sugar
5ml of pure honey

Ask patient to identify cause of hypoglycemia and try to avoid such incidents.
•Should carry fast sugar around

  • Nil per os if confused or unconscious
  • Should follow up with complex carbohydrate and proteins

15/15 rule

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

Explain the 15/15 rule

A

Should check blood sugar levels in 15min, if less than 5mmol/l, should repeat 15mg of sugar until normal levels is attained

•Contact medical care provider if the more than 3 hypoglycemic episodes per week

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

How is hypoglycemia managed in an unconscious patient

A

25mls -» of 50% dextrose till the patient is conscious
•Then set up 5% dextrose

Glucagon1mg subq,IM,IV follow with intravenous or oral carbs
Action:hormone -raises BS levels
Onset of 10 minutes
Duration of 25minutes
Position -side lying
S/E: N/V
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is hypoglycemia considered gerontological

A

Cognitive defects - not recognize S and S

Decreased renal function-oral hypoglycemic meds stay longer in the body

More likely to skip a meal

Vision problems-inaccurate insulin draws

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

What are the nursing measures in hypoglycemia

A
Follow protocol
Carry simple sugars at all times
S and S or hypoglycemia 
How to prevent hypoglycemia 
Check FSBS if you suspect 
Encourage to wear ID bracelet 
Teach family that belligerence(hostile attitude and aggressiveness) is a sign of hypoglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is DKA
Which type does it usually occur in
At what sugar level does it occur at

A

Serious complication of dm
•Usually occurs usually with type 1 but can also occur with type 2
•Usually occurs at sugars levels above 14mmol/l

29
Q

What is the physiology of DKA

Three sentences please

A

Results from breakdown of fat and overproduction of ketones by the liver and loss of bicarbonate

30
Q

Causes of DKA or etiology

A

Illness
Infection
Stress(physical or emotional)
Number 1causes are the above

Trauma
Surgery 
Pregnancy 
Absence or inadequate insulin
-taking too little insulin
-omitting doses of insulin

A known diabetic that has increased energy needs
Initial or undiagnosed diabetes
Developing insulin resistance

31
Q

What are the clinical features of DKA

A

Hyperglycemia
Dehydration
Electrolyte loss
Metabolic acidosis

32
Q

What is the pathophysiology of DKA

A

When there isn’t enough insulin glucose stays in the blood and this causes DKA in two mechanisms 1. so muscles don’t get enough energy causing increased fat metabolism leading to increased ketones in the blood causing metabolic acidosis leading to decreased serum pH and increased respiratory rate or 2. Glucose bunch in the blood causes hyperglycemia causing osmotic diuresis (causing electrolyte loss )leading to polyuria (this also causes electrolyte loss) and polydipsia leading to dehydration

33
Q

What are the signs and symptoms (S and S) of DKA

A
Hyperglycemia 
-it increases blood glucose
-person gets tired easily
Polyphagia 
Decreased attention,confusion
N/V,abdominal pain
Blurred vision 
Dehydration 
-polydipsia 
Polyuria 
Dry/flushed skin
Orthostatic hypotension 
Tachycardia 
Headaches 
Decreased sodium and potassium levels
34
Q

How is DKA diagnosed using blood and urine

What do you check for in the blood and urine and what are the results to see to diagnose DKA

A

Blood:
1.Serum osmolality
It is increased
And it’s thick

2.Ketones
They’re positive

3.bicarbonate
It is reduced
It’s less than 15mEq/L

4.pH
It’s reduced
Less than 7.3

5.sugar levels
They’re elevated
Greater than 250 mg/dL

  1. BUN Blood urea
    Nitrate

7.increased
Dehydration

Urine

  1. ketones are present
  2. glucose is present
  3. specific gravity of urine is decreased
35
Q

How is DKA managed

A
Focus on the four main clinical features 
Hyperglycemia 
Dehydration 
Electrolyte loss
Acidosis
36
Q

Alterations in blood sugar causes?

How does the blood sugar affect large blood vessels (macro circulation) and small blood vessels(microcirculation)

A

It causes hyperglycemia and hypoglycemia

Macro-
Atherosclerosis occurs more frequently earlier in diabetics
Involves coronary,peripheral, and cerebral arteries

Micro-
Affects basement membrane of small blood vessels and capillaries
Involves tissues affecting eyes and kidneys

37
Q

When does HHNK occur (hyperglycemia hyperosmolar nonketonic syndrome)

It occurs in all types of diabetes especially which type

A

Occurs when there’s insufficient insulin to prevent hyperglycemia but there is enough insulin to prevent ketoacidosis

It occurs in all types of diabetes
Especially type 2

38
Q

What are the characteristics of HHNKS and what is the difference between it and DKA

A
Extreme hyperglycemia (800-2000mg/dl)
Undetectable ketonuria 
Absence of acidosis 

Major difference from diabetic ketoacidosis is the lack of ketonuria cuz there’s some residual ability to secrete insulin in NIDDM

39
Q

What are the precipitating factors of HHNKs

A
Infection (most common)
Therapeutic agent or procedure 
Acute or chronic illness 
Overeating 
Stress
Too little insulin
40
Q

Nursing responsibilities in HHNK

A
It’s the same as DKA
Insulin
Hydration 
Electrolyte replacement and monitoring 
Treat underlying cause
41
Q

What are the acute complications of DM

A

Hypoglycemia
DKA
HHNKS

42
Q

State four macrovascular and microvascular complications ( chronic complications of diabetes)

A

~~~
Macrovascular ( Post prandial glucose)
-Arteriosclerosis
This is characterized by thickening and loss of elasticity of the arterial walls “hardening of the arteries “

-coronary artery disease( the heart): high blood pressure and insulin resistance and increases risk of coronary heart disease

-cerebrovascular disease( the brain):increased risk of stroke
-peripheral vascular disease ( the peripheries)( narrowing of blood vessels increases risk for reduced blood flow to legs

Microvascular :(Fasting glucose )
- characterized by basement membrane thickening
- affects smallest blood vessels
- due to hyperglycemia

Eye:high blood fluid and high blood pressure damages eye blood vessels causing retinopathy and cataract and glaucoma

Kidney:
High blood pressure damages small blood vessels and excess blood glucose overworks the kidneys resulting in Nephropathy

Nerves:
Hyperglycemia damages nerves in the eprioheral nervous system

43
Q

Cardiovascular disease is the major source of mortality in patients with type 2 DM true or false

A

True

44
Q

Two thirds of people with diabetes due of heart disease or stroke
Men with diabetes face a 2fold increased risk for CHD and women have a 3fold to 4fold increased risk
Diabetics are more likely to develop MI,Congestive Heart failure
True or false

A

True

45
Q

How are the complications prevented

A

Managing diabetes
Lowering risk factors for conditions
Routine screening for complications
Implementing early treatment

46
Q

What is the physiology of the pancreas (what the pancreas produces and the functions of what is produced
Where is the pancreas located?

A

The pancreas is a dual-functional gland, with both exocrine (digestive) and endocrine (hormonal) functions.

In this article, we shall look at the endocrine functions of the pancreas and their clinical significance.
Cells of the Pancreas
The pancreas is a partially retroperitoneal, abdominal organ found posterior and inferior to the stomach. Further information on the anatomy of the pancreas can be found here.

There are a variety of cell groups within the pancreas. Firstly, there are clusters of cells known as Islets of Langerhans. These islets contain the cell types that produce the hormones relating to the endocrine functions of the pancreas. There are also acini and duct systems within the pancreas, which are responsible for producing enzymes relating to the exocrine functions of the pancreas.

Islets are thought to make up 5% of the overall volume of the pancreas, although they receive around 15% of its blood flow. The Islets of Langerhans contain the following cell types:

Alpha cells – these make up roughly 15-20% of Islet cells and are responsible for producing glucagon
Beta cells – these make up 65-80% of Islet cells and produce insulin and amylin
Delta cells – these make up 3-10% of Islet cells and produce somatostatin
Gamma cells – these make up 3-5% of Islet cells and are responsible for production of pancreatic polypeptide
Epsilon cells – these make up less than 1% of Islet cells and produce ghrelin
By User:Polarlys (Own work) CC BY 2.5 (http://creativecommons.org/licenses/by/2.5)], via Wikimedia Commons

Fig 1 – The lighter tissue in this section is the Islet cells. The darker staining tissue is pancreatic acini.
Pancreatic Hormones
Pancreatic hormones are produced in the Islets of Langerhans. Scattered throughout exocrine tissue in the tail of the pancreas, these are spherical groups of different cell types producing different polypeptide hormones.

There are 6 key polypeptide hormones secreted by the endocrine pancreas. The table below summarises the cells that produce these and the main functions of these hormones:

1.Pancreatic Hormone 2.Produced by 3.Function
1.Insulin 2.Beta cells 3.Decrease blood glucose levels
1.Amylin 2.Beta cells 3.Slows gastric emptying to prevent spikes in blood glucose levels
1.Glucagon 2.Alpha cells 3.Increase blood glucose levels
1.Somatostatin 2.Delta cells 3.Regulates Islet cell secretion of other hormones
1.Pancreatic Polypeptide 2.Gamma cells 3.GI function
1.Ghrelin 2.Epsilon cells 3.Increase in appetite
These hormones can also regulate the action of other cell types within the Islets.

Insulin stimulates action of beta cells and inhibits alpha cells.
Glucagon stimulates action of alpha cells, which in turn then leads to activation of beta and delta cells
Somatostatin leads to inhibition of both alpha and beta cells.

Clinical Relevance
Type 1 Diabetes Mellitus

Diabetes Mellitus is an endocrine disorder characterised by chronic hyperglycaemia due to either insulin resistance and/or insulin deficiency. Type 1 Diabetes Mellitus mainly affects younger people <30 years

There is absolute insulin deficiency due to autoimmune destruction of pancreatic beta cells. This means that the beta cells are recognised as “foreign” or “non-self” by the body and so are attacked and destroyed by the body’s immune system.

Viral infection in a young person with pre-disposing factors, e.g. family history, is a common trigger. In some cases there is relative insulin deficiency due to defective Beta cells and inadequate insulin secretion or rate of secretion.

Commonly, Type 1 Diabetes Mellitus presents with a classic triad of symptoms: polyuria, polydipsia and weight loss. Due to the lack of insulin being produced by the body in Type 1 Diabetes, patients must be treated with injectable insulin regime.

The average age of diagnosis in the UK is between 10 and 14 years, therefore effective patient education forms an important part of treatment for this disease. It is a lifelong disease which needs tight control of glucose levels and explaining the importance to children and young adults can be challenging.

47
Q

State ten causes of pancreatitis

A

Pancreatitis refers to inflammation of the pancreas – this is can be acute or persist over an extended period (chronic pancreatitis). The causes of pancreatitis can be remembered using the mnemonic – GET SMASHED:

Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion stings
Hypertriglyceridemia, hypercalcaemia and hyperparathyroidism
ERCP – endoscopic retrograde cholangiopancreatography
Drugs – such as sodium valproate, azathioprine and sulphonamides
Pancreatitis creates severe epigastric pain which often radiates to the back, nausea, vomiting and diarrhoea.

Treatment involves supportive measures such as IV fluids and analgesia. Antibiotics are rarely required, as most cases are not due to infection. The underlying cause will then also need to be treated.

48
Q

What is the anatomy of the pancreas

A

Anatomical Position
The pancreas is an oblong-shaped organ positioned at the level of the transpyloric plane (L1). With the exception of the tail of the pancreas, it is a retroperitoneal organ, located deep within the upper abdomen in the epigastrium and left hypochondrium regions.

Within the abdomen, the pancreas has direct anatomical relations to several structures

Organs:

Stomach – Separated from the pancreas by the lesser sac, the stomach and pylorus lie anterior and to the pancreas.
Duodenum – The “C” shaped duodenum curves around and outlines the head of the pancreas. The first part of the duodenum lies anteriorly whereas the second part of the duodenum including the ampulla of Vater lies laterally to the right of the pancreatic head
Transverse mesocolon – Attaches to the anterior surface of the pancreas
Common bile duct – Descends behind the head of the pancreas before opening into the second part of the duodenum alongside the major pancreatic duct through the major duodenal papilla
Spleen – located posteriorly and laterally. The lienorenal ligament is formed from peritoneum and connects the spleen to the tail of the pancreas.
Vessels

The pancreas lies near several major vessels and significant landmarks in vascular anatomy:

The aorta and inferior vena cava pass posteriorly to the head of the pancreas.
The superior mesenteric artery lies behind the neck of the pancreas and anterior to the uncinate process.
Posterior to the neck of the pancreas, the splenic and superior mesenteric veins unite to form the hepatic portal vein.
As it journeys from its origin at the celiac plexus to the splenic hilum, the splenic artery traverses the superior border of the pancreas.
By TeachMeSeries Ltd (2023)

Fig 1 – Anterior view of the abdomen. The stomach, transverse colon, and the majority of the small intestine have been removed to expose the underlying pancreas
Anatomical Structure
The pancreas is typically divided into five parts:

Head – the widest part of the pancreas. It lies within the C-shaped curve created by the duodenum and is connected to it by connective tissue.
Uncinate process – a projection arising from the lower part of the head and extending medially to lie beneath the body of the pancreas. It lies posterior to the superior mesenteric vessels.
Neck – located between the head and the body of the pancreas. It overlies the superior mesenteric vessels which form a groove in its posterior aspect.
Body – centrally located, crossing the midline of the human body to lie behind the stomach and to the left of the superior mesenteric vessels.
Tail – the left end of the pancreas that lies within close proximity to the hilum of the spleen. It is contained within the splenorenal ligament with the splenic vessels. This is the only part of the pancreas that is intraperitoneal.
By TeachMeSeries Ltd (2023)

Fig 2 – The parts of the pancreas
Duct System

The exocrine pancreas is classified as a lobulated, serous gland which produces digestive enzyme precursors. It is composed of approximately one million ‘berry-like’ clusters of cells called acini, connected by short intercalated ducts.

The intercalated ducts unite with those draining adjacent lobules and drain into a network of intralobular collecting ducts, which in turn drain into the main pancreatic duct.

The pancreatic duct runs the length of the pancreas and unites with the common bile duct, forming the hepatopancreatic ampulla of Vater. This structure then opens into the duodenum via the major duodenal papilla.

Secretions into the duodenum are controlled by a muscular valve – the sphincter of Oddi. It surrounds the ampulla of Vater, acting as a valve.

By TeachMeSeries Ltd (2023)

Fig 3 – The exocrine pancreas, secreting into the duodenum
Vasculature
The pancreas is supplied by the pancreatic branches of the splenic artery. The head is additionally supplied by the superior and inferior pancreaticoduodenal arteries which are branches of the gastroduodenal (from coeliac trunk) and superior mesenteric arteries, respectively.

Venous drainage of the head of the pancreas is into the superior mesenteric branches of the hepatic portal vein. The pancreatic veins draining the rest of the pancreas do so via the splenic vein.

By TeachMeSeries Ltd (2023)

Fig 4 – The arterial supply and venous drainage of the pancreas
Lymphatics
The pancreas is drained by lymphatic vessels that follow the arterial supply. They empty into the pancreaticosplenal nodes and the pyloric nodes, which in turn drain into the superior mesenteric and coeliac lymph nodes

49
Q

How is MODY diagnosed?

A

For patients with diabetes diagnosed before 25years,
1. First check if it was diagnosed before 6 months
If yes, do a genetic test for neonatal diabetes cuz there’s a likelihood that it’s a possible neonatal diabetes

  1. Was there abrupt onset of ketoacidosis? While the patient is not obese? While that patient has insulin deficiency?
    If yes,check for beta cell autoantibodies
    If the antibodies are positive, there’s a possible type 1 diabetes
    If no, it’s Yong onset diabetes in at least the second generation
  2. Is there obesity? Is there insulin resistance? Are there negative beta autoantibodies ?
    If yes, it’s a possible type 2 diabetes
    If no, there is negative beta cell autoantibodies and it’s Yong onset diabetes in at least the second generation
    Do genetic testing for MODY
    IF POSITIVE, it’s a possible MODY
50
Q

Explain the ominous octet of diabetes mellitus

A

Type 2 diabetes is characterized by multiple pathophysiologic abnormalities which collectively have been referred to as the Ominous Octet

The Ominous Octet of obesity is an organ-system based rubric, which helps in identification of various sites of dysfunction in a person living with obesity.

Ominous Octet:( all these cause hyperglycemia)
1. Impaired peripheral glucose uptake from the muscles-the receptors on your liver and muscle cells do not function properly to take up glucose, causing glucose to remain in the bloodstream
2.Increased glucose reabsorption by the kidneys-in an attempt to conserve glucose as an energy source, the kidneys hold onto more of it which keeps blood levels high
3.increased lipolysis by fatty tissue and insulin resistance -increased fat breakdown raises triglycerides in the blood which can impair insulin secretion
4.Decreased incretin effect in intestines-gut hormones that normally stimulate insulin secretion in response to food are less effective and produced at lower quantities
5.Impaired insulin secretion by pancreas
6.increased glucagon secretion by pancreas-higher levels of glucagon (a hormone) trigger the production of glucose (sugar)
7. Increased hepatic glucose production by liver -your liver dumps out too much glucose (sugar)
8.neurotransmitter dysfunction by brain-altered neurotransmitter function in your brain which does not properly trigger the sensation of feeling full (appetite)

.

51
Q

How is DM diagnosed
How is impaired glucose tolerance diagnosed?
How is impaired fasting glucose diagnosed?

A

Diabetes:
Fasting plasma glucose- more than or equal to 7.0mmol/L or 126mg/dL

Or two hour plasma glucose after 75g anhydrous oral glucose load dissolved in water (OGTT) more than or equal to 11.1 mmol/L or 200mg/dL

Or HbA1C more than or equal to 48mmol/mol equivalent to 6.5%

Or random plasma glucose in the presence of hyperglycemia and more than 11.1 mmol/mol or 200mg/dL

Impaired glucose tolerance diagnosed:
For it to be diagnosed, two of the criteria must be met:
a. Fasting plasma glucose Less than 7mmol/L and
b. two hour plasma glucose after 75g oral glucose load (OGTT) less than 11.1 mmol/L and more than or equal to 7.8mmol/L
Or 140-200mg/dL

How is impaired fasting glucose diagnosed-
Should be diagnosed if the first or both are met:
Fasting plasma glucose 6.1-6.9 mmol/L (110-125mg/dL) and
b. two hour plasma glucose after 75g oral glucose load (OGTT) less than 7.8 mmol/L
Or 140mg/dL

52
Q

Explain how glycated haemoglobin is formed
How many days does a red blood cell live in the blood
Where is hemoglobin found?
In adults, how many forms of Hb exist and name them and which is more predominant

A

120days
Hb is found in the blood cell
Glucose or sugar enters in the bloodstream and into the rbc
It binds to the Hb in the rbc
This binding creates glycated hemoglobin

Forms of Hb: Hb A1, Hb A2, Hb F
Hb A1 is predominant

Glycated hemoglobin means a chemically stable conjugate of any of the forms of Hb with glucose

Glycated forms of hemoglobin are formed slowly irreversibly and non enzymatically at a rate that is proportional to the concentration of glucose in the blood

53
Q

State. glycated haemoglobin pros and cons

A

Pros:
Chronic hyperglycemia is caught more accurately by HbA1C than FPG

Fasting is not needed for A1C assessment

No acute perturbation (smoking, stress, diet, exercise) affect A1C

Individual susceptibility to protein glycation might be A1C

A1C can be used concomitantly for diagnosing and initiating monitoring of diabetes

Cos:
Diabetes is clinically defined as elevated blood glucose and not elevated glycated proteins

2hours level glucose and Impaired glucose tolerance are stronger than A1C

Standardization of A1C assay is poor compare to glucose assay

A1C of 6.0-6.5% do not predict diabetes as accurately as fasting plasma glucose and 2hour plasma glucose (OGTT)

A1 levels vary not only according to glycemia but also according to erythrocyte turnover rates( examples are hemoglobiopathies , malaria, blood loss)

A1C varies in ethnic groups

54
Q

Explain four conditions that affect HbA1C ( whether they falsely lower or falsely increase it and why) ?

A

Erythrocyte lifespan(factor)
Falsely lower- decrease erythrocyte lifespan ( splenomegaly, recent blood transfusion, hemolytic anemia)

Falsely increase- increased erythrocyte lifespan ( splenectomy)

Erythropoiesis:
Falsely lower(reticulocytosis , erythropoietin administration)
Falsely increase(Iron/B12 deficiency ,decreased erythropoiesis

Assay interference:
Falsely elevated- chronic alcoholism
Falsely decreased-severe hypertriglyceridemia

Glycation-
Falsely lowered: high dose vitamin C or E
Falsely elevated : chronic kidney disease

55
Q

How is the 2 hour post pea dial glucose performed

A

2 hour plasma glucose- fasts for two hours
Blood is taken
After five minutes , they take glucose preparation
One hour after drinking they take blood sugar
Two hours after drinking. They take blood sugar

56
Q

What are the stages of diabetic retinopathy

A

Mild non proliferative DR
Moderat en hon proliferative
Severe non proliferative
Proliferative DR

All these can lead to vitreous haemorrhage and traction retinal detachment and macular edema

In non proliferative DR, there is haemorrhage, hard exudates,aneurysm and in proliferative DR, there are abnormal blood vessels

57
Q

How does painless and then painful diabetic neuropathy occur
State the risk factors associated wi tbh developing painful neuropathy

A

DM with hyperglycemia, dyslipidemia and altered insulin signaling can cause microvascular and metabolic changes.
Microvascular chnages lead to reduced perfusion and nerve ischaemia. This leads to structural and functional alterations of peripheral nerves thus leading to painless diabetic neuropathy

The metabolic CHanges lead to hyperactivity of several pathways such as 1. polyol pathway, the polyol pathway activation could be the primary cause of oxidative stress associated with diabetes. However, oxidative stress could be also initiated by autoxidation of glucose and their metabolites, 2.increased intracellular formation of AGEs, increased expression of the receptor for AGEs and its activating ligands, altered mitochondrial function, activation of 3.PKC isoforms and overactivity of the 4.hexosamine pathway.
All these pathways lead to oxidative stress, mitochondrial dysfunction and inflammation. These three also lead to
structural and functional alterations of peripheral nerves thus leading to painful diabetic neuropathy.

Risk factors for developing painful neuropathy include:
Obesity, female gender, genotype and glycemic burden

Other factors include reduced vitamin D,reduced blood flow

58
Q

Explain the Wagner classification of diabetic foot ulcers

A

Grade 0- no ulcer in a high risk foot
1- superficial ulcer involving the full skin thickness but not the underlying tissues
2-deep ulcer penetrating down to the muscles and ligaments but no bone involvement or abscess formation
3-deep ulcer with cellulitis or abscess Formation often with osteomyelitis
4- localized gangrene
5-extensive gangrene involving the whole foot

59
Q

Explain in simple terms diabetic Nephropathy

A

Poor glycemic control leads to increased blood pressure, increased blood volume and increased renal perfusion
This causes initial increased GFR which causes stress to the glomerulus and leads to pressure induced damage
This leads to podocyte injury and makes the glomerular basement membrane to be permeable to proteins leading to albuminuria

This leads to protein endocytosis into tubular cells leading to inflammation
This leads to tubular fibrosis leading to scarred glomeruli which are not able to filter blood properly anymore
Leading to reduced GFR and diabetic Nephropathy

60
Q

Generally, how is diabetes managed

A

1.control fasting and postprandial sugars
2.reach targets HbA1C , Lipids and BP
3.avoid weight gain
4. Treat macro and micro complications and non vascular complications

61
Q

How often do you screen for the following complications in diabetes
Retinopathy, diabetic neuropathy, Nephropathy, lipids, HbA1C,CAD

A

Screen for retinopathy- do a dilated eye examination annually

Examination of the feet-inspect feet at each visit and do thorough feet examination annually

Monitor HbA1C every three months until you reach the target you want
Monitor every six months after you reach the target

Measure fasting lipids annually

Measure urine albumin-to creatinine ratio annually

Do additional screening for Coronary artery disease (BP check, smoking history and exercise history) at each visit

62
Q

For each ominous octet(do for the muscles, kidney and lipolysis) , state the drugs used to treat it and how they work

A

Ominous Octet:( all these cause hyperglycemia)
1. Impaired peripheral glucose uptake from the muscles-the receptors on your liver and muscle cells do not function properly to take up glucose, causing glucose to remain in the bloodstream

a.Metformin-increases uptake of glucose by liver and muscles and counters insulin resistance
b.insulin-increases uptake of glucose by liver and muscles and storage and metabolism by liver, suppresses glucose production and decreases lipolysis
c.thiazolidinediones (pioglitazone,rosiglitazone)- increases insulin sensitivity

2.Increased glucose reabsorption by the kidneys-in an attempt to conserve glucose as an energy source, the kidneys hold onto more of it which keeps blood levels high

a.SGLT2 (sodium glucose cotransporter 2) inhibitors (canagliflozin, dapagliflozin, and empagliflozin.)-preventing the kidneys from reabsorbing glucose back into the blood. This allows the kidneys to lower blood glucose levels and the excess glucose in the blood is removed from the body via urine.

3.increased lipolysis by fatty tissue and insulin resistance -increased fat breakdown raises triglycerides in the blood which can impair insulin secretion and increase risk of atherosclerosis
a. thiazolidinediones (pioglitazone,rosiglitazone)- increases insulin sensitivity because
Insulin promotes lipogenesis, thereby resulting in the storage of triglycerides in adipocytes and of low-density lipoproteins (LDL) in hepatocytes. Insulin favours the storage of fat in adipose tissue by 3 mechanisms: — 1. it inhibits lipolysis; — 2. increases the glucose uptake, lipogenesis and reësterification of free fatty acids; — 3.

63
Q

For each ominous octet(do for thepancreas’s ,intestines, liver and brain and) , state the drugs used to treat it and how they work

A

4.Decreased incretin effect in intestines-gut hormones that normally stimulate insulin secretion in response to food are less effective and produced at lower quantities. Incretins are gut-derived hormones, members of the glucagon superfamily, released in response to nutrient ingestion, mainly glucose and fat. They stimulate pancreatic insulin secretion. Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are the two most important hormones
By stimulating insulin secretion in a glucose-dependent manner, they ensure that postprandial glucose levels do not increase excessively.

a. Metformin- increase glucose uptake and counters insulin resitance
b. Colesevelam-Colesevelam, a bile-acid sequestrant, lowers glucose levels in patients with type 2 diabetes mellitus (T2DM) by a mechanism that is associated with increased incretin secretion and improved β-cell function, but not with reduced gluconeogenesis or glucose absorption.
c.alpha glucosidase inhibitors-Alpha-glucosidase inhibitors are antihyperglycemic agents that lower blood glucose by delaying the digestion and absorption of complex carbohydrates. Alpha-glucosidase inhibitors (AGIs; acarbose, miglitol, voglibose). AGIs delay the absorption of carbohydrates from the small intestine and thus have a lowering effect on postprandial blood glucose and insulin levels

5.Impaired insulin secretion by pancreas-
a.Sulfonylurea(Glimepiride,Glyburide
Glipizide ) -stimulate insulin secretion
b.meglitinide:stimulate insulin secretion (There are three available drugs: repaglinide, nateglinide, and mitiglinide.)
c.GLP-1 receptor agonist:increase incretin effect. These agents work by activating GLP-1 receptors in the pancreas, which leads to enhanced insulin release and reduced glucagon release-responses. Examples ;Dulaglutide
Exenatide extended release
Exenatide
Semaglutide
Liraglutide
Lixisenatide
Semaglutide
d. DPP-4 inhibitors:increase incretin effect. DPP-4 inhibitors work by blocking the action of DPP-4, an enzyme which destroys the hormone incretin. sitagliptin, saxagliptin, linagliptin, and alogliptin

6.increased glucagon secretion by pancreas-higher levels of glucagon (a hormone) trigger the production of glucose (sugar)

a.GLP-1 receptor agonist:increase incretin effect. These agents work by activating GLP-1 receptors in the pancreas, which leads to enhanced insulin release and reduced glucagon release-responses. Examples ;Dulaglutide
Exenatide extended release
Exenatide
Semaglutide
Liraglutide
Lixisenatide
Semaglutide
b.DPP-4 inhibitors:increase incretin effect. DPP-4 inhibitors work by blocking the action of DPP-4, an enzyme which destroys the hormone incretin. sitagliptin, saxagliptin, linagliptin, and alogliptin
c. Amylin-In the pancreas, amylin inhibits the release of glucagon and thus decreases blood glucose via inhibition of hepatic glucose production.

  1. Increased hepatic glucose production by liver -your liver dumps out too much glucose (sugar)

Metformin-increases uptake of glucose by liver and muscles and counters insulin resistance
b.insulin-increases uptake of glucose by liver and muscles and storage and metabolism by liver, suppresses glucose production and decreases lipolysis
c.thiazolidinediones (pioglitazone,rosiglitazone)- increases insulin sensitivity

8.neurotransmitter dysfunction by brain-altered neurotransmitter function in your brain which does not properly trigger the sensation of feeling full (appetite)

a. Amylin-In the pancreas, amylin inhibits the release of glucagon and thus decreases blood glucose via inhibition of hepatic glucose production. Example pramlintide is an amylin analogue
b. GLP-1 receptor agonist:increase incretin effect. These agents work by activating GLP-1 receptors in the pancreas, which leads to enhanced insulin release and reduced glucagon release-responses. Examples ;Dulaglutide
Exenatide extended release
Exenatide
Semaglutide
Liraglutide
Lixisenatide
Semaglutide
c. Bromocriptine is thought to act on the circadian neuronal activities in the hypothalamus, to reset an abnormally elevated hypothalamic drive for increased plasma glucose, free fatty acids, and triglycerides in insulin-resistant patients.it is a dopamine receptor agonist

64
Q

How is type 2 diabetes managed (5 steps)

Why won’t you add insulin to a SU drug

A
  1. Get diabetes education,monitor blood glucose and make the lifestyle changes
    2.Add a medicine:metformin or blood glucose normalizing medicine
  2. After 3-6 months if patient is not doing well on metformin, add either insulin or another oral medication
    Step4. If still, add another oral med or insulin
    Step5 : If patient is on three oral meds but still nothing is helping , consider insulin intensified therapy with or without the previous oral meds

No insulin to an SU cuz it can cause hypoglycemia

65
Q

So in a patient with cost being an issue and without established CKD or ASCVD, what drugs do you give and what to do you give if they’re not working

A

First give SU or give a TZD
If the SU isn’t working then you switch to a TZD
If you started with a TZD and it’s not work then switch to an SU

If after switching neither is working then switch to low cost insulin
Or DPP-4 inhibitors or SGLT2 inhibitors

66
Q

So in a patient with cost not being an issue and with established CKD orHF, what drugs do you give and what to do you give if they’re not working
Why would you Avoid TZD in the setting of HF

A

Start SGLT2 inhibitors with evidence of reducing HF and or CKD progression of eGFR is adequate

If SGLT2 inhibitors are not tolerated or are contraindicated or if eGFR loss is less than adequate then add GLP-1 agonist

Avoid TZD in the setting of HF
However,TZDs increase renal sodium and water reabsorption, leading to fluid retention and overt signs of HF in patients with diabetes.

66
Q

So in a patient with cost not being an issue and with established CKD orHF, what drugs do you give and what to do you give if they’re not working
Why would you Avoid TZD in the setting of HF

A

Start SGLT2 inhibitors with evidence of reducing HF and or CKD progression of eGFR is adequate

If SGLT2 inhibitors are not tolerated or are contraindicated or if eGFR loss is less than adequate then add GLP-1 agonist

Avoid TZD in the setting of HF
However,TZDs increase renal sodium and water reabsorption, leading to fluid retention and overt signs of HF in patients with diabetes.

67
Q

For diabetic combinations, which of the following drugs can be added to it to make a triple therapy combo

SGLT2i ,DPP-4 inhibitor,GLP-1 agonist, TZD,SU

A

For Metformin + SU, you can give all the drugs except adding another SU

Metformin + SGLT2 i, you can give all except SGLT2 i

Metformin + DPP-4 i, you can give all except DPP-4 i and GLP-1 agonist

Metformin + GLP-1 agonist, you can give all except GLP-1 agonist and DPP-4 i

Metformin + TZD, you can give all except TZD

Metformin + basal ( not intensive) insulin , you can give all except SU

68
Q

Name the types of mixture and when they are given

A

Fast acting (soluble) and long acting (isophane) insulin

Mixtard is a suspension for injection that contains

Mixtard is given 30mins before meals

Mixtard 30: soluble insulin 30% and isophane 70%
Mixtard 40: soluble insulin 40% and isophane 60%

Mixtard 50: soluble insulin 50% and isophane 50%