DIABETES [S] Flashcards
1
Q
location is behind the stomach and in front of the spine
surrounded with liver, gallbladder and spleen
A
PANCREAS
2
Q
Size of PANCREAS
A
6 inches long
3
Q
widest part OF THE PANCREAS
A
Head
4
Q
→right side of the pancreas
A
Head
5
Q
Part:
sits at the curvature of the first segment of the small intestine or the duodenum
A
Head
6
Q
parts:
→short part of the pancreas
→extends from the head
A
Neck
7
Q
parts:
→middle part between head and neck
→extends upwards
A
Body
8
Q
parts:
left side of the pancreas
→located near the spleen
A
Tail
9
Q
parts:
thinnest part
A
Tail
10
Q
T/f
Pancreas is part of digestive system
A
T
11
Q
It is an organ in the back of your abdomen and a gland
A
PANCREAS
12
Q
helps with digestion and control blood sugar
A
PANCREAS
13
Q
two main functions of pancreas:
A
Exocrine Function
Endocrine Function
14
Q
produces substances (enzymes) that help with digestion
A. Exocrine Function
B. Endocrine Function
A
A
15
Q
sends out (hormones) that control the amount of
sugar in your bloodstream
A. Exocrine Function
B. Endocrine Function
A
B
16
Q
the pancreas secretes digestive enzymes as well as _____,
_____and ___, into the bloodstream to control the amount of glucose in the body
A
hormones, insulin, glucagon
17
Q
T/f
insulin lowers the level of blood glucose by allowing blood
glucose to enter the body cells where it is metabolized
A
T
18
Q
if the blood glucose is too low, glucagon stimulates the release
of glucose from the ____
A
liver
19
Q
after a meal, the glucose and amino acids are directly
absorbed into the bloodstream, blood glucose levels rises
sharply, and this increase of blood glucose will signal ____ of pancreas to secrete insulin into the bloodstream
A
Beta cells
20
Q
Lipase
Amylase
Protease
A
EXOCRINE GLAND
21
Q
enzymes → break down food (digestion)
A
EXOCRINE GLAND
22
Q
works with bile (liver) to break down fats
A. Lipase
B. Amylase
C. Protease
A
A
23
Q
breaks down carbohydrates for energy
A. Lipase
B. Amylase
C. Protease
A
B
24
Q
breaks down proteins
A. Lipase
B. Amylase
C. Protease
A
C
25
Insulin
Glucagon
ENDOCRINE GLAND
26
hormones that control blood sugar (glucose)
ENDOCRINE GLAND
27
reduces high blood sugar levels
A. Insulin
B.Glucagon
A
28
increases low blood sugar levels
A. Insulin
B.Glucagon
B
29
T/f
ENDOCRINE GLAND
the body needs a balance in its sugar to help the kidneys, liver,
brain, heart, circulatory system and nervous system
T
30
according to WHO, diabetes is a group of chronic metabolic
disease characterized by:
o high plasma blood glucose
o result from defective insulin secretion, action or both →
body unable to metabolize CHO, fats, CHONs
31
<140 mg/dL
3.5-8 mmol/L
below 6%
Normal
Glucose
32
140-199 mg/dL
7.8-11 mmol/L
6.0-6.4%
Prediabetes
33
200 or higher
11.1 mmol/L
6.5% or over
Diabetes
34
”glycated hemoglobin”
HbA1C
35
T/f
if blood sugar level has been high during recent weeks, HbA1C
will also be greater
T
36
the aimed level of HbA1C for diabetics is ____% or 48 mmol/L
the normal Hba1C is 6%
6.5
37
improving this by 1% for people with Type I or II diabetes will
lower the risk for microvascular complications by 25%
HbA1C
38
is a multi-systemic disease with a strong correlation
with cardiovascular disease development
Type II DM
39
this will lead to 2-4 times increase in the mortality rate of a
patient (cardiac disease, stroke, coronary artery disease,
cerebrovascular disease)
Type II DM
40
affects the small blood vessels:
o retinopathy
o nephropathy
o neuropathy
MICROVASCULAR
41
affects the large blood vessels:
o coronary artery disease
o cerebrovascular disease
o peripheral vascular disease
MACROVASCULAR
42
affects the motor, sensory and cranial as well as autonomic
nerves:
o polyneuropathy
o diabetic amyotrophy
o autonomic neuropathy
NEUROPATHIES
43
common concern of diabetes especially with poorly controlled
glucose levels
FOOT ULCERS
44
→skin disorders
→especially found in lower extremities
DERMOPATHIES
45
red, puffy hard patches on the legs
LIPOIDICA NECROBIOSIS
46
→skin around it has a gleaming porcelain like finish
→blood vessels can be seen
→skin is easily irritated and inflamed
LIPOIDICA NECROBIOSIS
47
dark patches of the skin that is velvety
→usually seen on back of the neck and around armpit
ACANTHOSIS NIGRICANS
48
common prediabetic or insulin resistance complication
ACANTHOSIS NIGRICANS
49
hardening or thickening of affected skin of the fingers, toes, or both
DIGITAL SCLEROSIS
50
T/f
DIGITAL SCLEROSIS has
swollen appearance, feels like sandy, pebbles on fingertips
T
51
orange peel in texture
DIGITAL SCLEROSIS
52
bullosis diabeticorum or diabetic bullae
BLISTERS
53
→typically appear on the hand
→not painful
→infections of the skin have a hot, swollen, itchy rash common
between toes or scalp
→patients may have open wounds or sores because of poor blood
circulation and nerve damage
BLISTERS
54
brown spots that may develop anywhere in the body especially
in the shin border of the lower extremity
→ these can disappear in a year or two if the sugar is well
controlled
DIABETIC DERMOPATHIES
55
small, reddish lumps on the skin
→ look like pimples
ERUPTIVE XANTHOMATOSIS
56
can be seen on the buttocks, thigh, elbows, back of the knees
and they become itchy and sensitive
→disappear when sugar is well controlled
ERUPTIVE XANTHOMATOSIS
57
→
elevated, raised red skin bumps
GRANULOMA ANNULARE
58
→
for diabetics, has an incidence rate of 3%
→
extremely dry, itchy due to high blood sugar and poor
circulation
GRANULOMA ANNULARE
59
→
scaly spots
→
body fat is too high
XANTHELASMA
60
LADA
Latent Autoimmune Diabetes in Adults
61
children and young adults (<30 years old); non-obese
TYPE I DIABETES MELLITUS
62
→
immune system destroys pancreatic B-cells
→
severe insulin deficiency
→
insulin resistance (occasional)
TYPE I DIABETES MELLITUS
63
→
islet cell antibodies are frequently present
→
associated with other autoimmune diseases
TYPE I DIABETES MELLITUS
64
→
ketosis is common
TYPE I DIABETES MELLITUS
65
→
5% of population
→
develops when the body’s immune system destroys the
pancreatic Beta cells
TYPE I DIABETES MELLITUS
66
→
islet cell antibodies absent
→
not associated with other autoimmune diseases
TYPE II DIABETES MELLITUS
67
ketosis not common
TYPE II DIABETES MELLITUS
68
causes:
o multifactorial
o risk factors:
-obesity
-lifestyle factors
-genetic predisposition
-gut symbiosis
-metabolic
→organs involved:
o pancreas
o liver
o skeletal muscle
o kidneys
o brain
o small intestine
o adipose tissue
TYPE II DIABETES MELLITUS
69
there are main factors which quadruple the incidence and
prevalence of Type II DM:
o global rise in obesity
o sedentary lifestyle
o high caloric diet (Western diet)
o aging population
70
usually begins as insulin resistance
TYPE II DIABETES MELLITUS
71
→a disorder in which the cells do not use insulin properly
→as the need of insulin rises, the pancreas gradually loses the
ability to produce insulin
TYPE II DIABETES MELLITUS
72
PATHOPHYSIOLOGICAL FACTORS
→adipokine dysregulation
→inflammation and abnormal gut microbiota
→immune dysregulation and inflammation
73
T/f
According to International Diabetes Federation (IDF) 2019:
→diabetes constitutes 4.2 million deaths
→around 40-59 years old
→low to middle income countries (80%)
→increase risk:
o coronary heart disease
o ischemic stroke
o other vascular disease
→risk factors:
o non-modifiable
o modifiable (can be controlled)
T
74
T/f
According to International Diabetes Federation (IDF) 2019:
→diabetes constitutes 4.2 million deaths
→around 40-59 years old
→low to middle income countries (80%)
→increase risk:
o coronary heart disease
o ischemic stroke
o other vascular disease
→risk factors:
o non-modifiable
T
75
non-modifiable risk factor
ETHNICITY AND FAMILY HEREDITARY
OR GENETIC PREDISPOSITION
76
→
Japanese, Hispanics, and Native Americans have the highest risk
→
higher incidence rates in Asians when compared with Native
Americans
→
higher risk in black population than white
ETHNICITY AND FAMILY HEREDITARY
OR GENETIC PREDISPOSITION
77
modifiable risk factor
OBESITY, LOW PHYSICAL ACTIVITY AND UNHEALTHY DIET
78
T/f
BMI > 30 kg/m2 (obese) → metabolic abnormality → insulin
resistance
T
79
chronic low-grade systemic inflammation
(IL6, CRP , TNF-a, IL1)
80
T/f
o walking 2-3 hours a week or at least 40 minutes reduces
the development of Type II DM by 34%
o there are primary benefits of physical activity in delaying
Type II DM onset:
-
contraction of skeletal muscle cells which can
induce an increase in blood flow and enhancing
glucose uptake from plasma
-
reduces intra-abdominal fat which lowers the risk
of insulin resistance
T
81
T/f
moderate to an increased exercise will improve glucose
uptake up to 40% and even reverse inflammation and
oxidative stress
82
T/f
a sedentary lifestyle will constitute link between obesity
and Type II DM and is associated with higher markers of
chronic low grade systemic inflammation or
proinflammatory molecules that are released into the
bloodstream and within specific tissues such as the IL-6, CRP ,
TNF-a, or IL-1
o these inflammatory markers produce a state called
metabolic inflammation
T
83
T/f
intentional weight loss remains the cornerstone therapy to
improve insulin sensitivity and prevent the incidence of Type II
DM:
o regular exercise
o increased physical activity (show reduced levels of IL-6,
IL-8, CRP , and leptin)
-
can improve Type II DM through inducing oxidative
stress by inducing the synthesis of anti-oxidant
Glutathione or GSH which is a major non-enzymatic oxidant leading to a long term
reduction in free radicals or ROS (reactive oxygen
species)
T
84
is a molecule associated with CRP (C-reactive protein).
Leptin
85
modulate immune system & inflammatory response
→
regulate gut barrier integrity & human metabolism
GUT MICROBIOTA
86
→
synthesis of metabolites
o these gut-resident microorganisms produce metabolites that
contribute to physiology of a healthy individual but due to
some inherited or acquired factors, such as age, nutrition,
lifestyle, genetic predisposition or any underlying disease, it
can affect the gut microbiota causing metabolic
disturbances that end up in disease
o recent studies indicate that changes in the gut symbiosis
causes imbalance or dysbiosis which can now promote
insulin resistance and Type II DM
GUT MICROBIOTA
87
high-fat diet induces 3x LPS production → low-grade
inflammation and insulin resistance
o hyperglycemia induces an excess of ROS generation by the
mitochondria which gives rise to diabetes complications that
may persist even when hyperglycemia is controlled
o a good glycemic control initiated very early on can prevent damage induced by hyperglycemia or oxidative stress which is not easily reversed when sugar is there for a long
time
GUT MICROBIOTA
88
→
refers to a low or a reduction in the metabolic response of
insulin or impaired/lower response to the circulating insulin by
the blood glucose level
→
decrease metabolic response of insulin-responsive cells
INSULIN RESISTANCE (IR)
89
T/f
categories of insulin resistance or insulin-deficient conditions:
o diminished insulin secretion by Beta cells
o insulin antagonists in plasma
o impaired insulin response in target tissues
-a defective action of insulin in these tissues often
precedes the development of systemic insulin
resistance leading to Type II DM
T
90
1. What is the role of insulin in healthy adipose (fat) tissue?
A) It increases inflammation and reduces glucose uptake
B) It stimulates glucose uptake and triglyceride synthesis
C) It prevents free fatty acid uptake
D) It stops macrophage activity completely
2. What happens in hypertrophic (enlarged) adipose tissue?
A) Glucose uptake increases
B) Free fatty acid release decreases
C) Hypoxia and inflammation increase
D) Macrophage activity is reduced
3. How does insulin regulate glucose and fat metabolism in the liver?
A) It only controls glucose levels, not fat metabolism
B) It binds to liver cells, triggering metabolic processes like glycogen synthesis
C) It increases glucose production in the liver
D) It works exactly the same as glucagon
4. What does glucagon do in the liver?
A) Inhibits glucose production
B) Stimulates glucose production
C) Reduces lipid synthesis
D) Enhances glycogen storage
5. What happens when there is insulin resistance in the liver?
A) Glycogen synthesis is impaired
B) Glucose production is suppressed
C) Lipogenesis (fat production) decreases
D) Pro-inflammatory molecules (CRP) decrease
6. How does insulin inhibit glucose production in the liver? (Short Answer)
7. What metabolic processes are regulated by insulin in the liver? (Short Answer)
1. Answer: B) It stimulates glucose uptake and triglyceride synthesis
2. Answer: C) Hypoxia and inflammation increase
3. Answer: B) It binds to liver cells, triggering metabolic processes like glycogen synthesis
4. Answer: B) Stimulates glucose production
5. Answer: A) Glycogen synthesis is impaired
6. Answer: Insulin signals the liver to store glucose as glycogen and prevents excessive glucose production, acting as a counterbalance to glucagon.
7. Answer: Insulin regulates glycogen synthesis, gluconeogenesis, glycolysis, and lipid synthesis to maintain blood sugar balance.
