Loading...
Question 1
What are the three anatomical regions of the pancreas?
Head, body, tail of pancreas
Question 2
From which week does the pancreas begin developing?
Week 4
Question 3
What is the origin of the pancreas and when does it start secreting insulin?
- ventral bud and dorsal bud with endoderm origin - secreting insulin from W10
Question 4
What are the endocrine functions of the pancreas?
- secretes hormones into the bloodstream - α- and β-cells producing insulin and glucagon → regulate blood sugar levels
Question 5
What are the exocrine functions of the pancreas?
- 90% of its functions as an exocrine gland - producing digestive enzymes
Question 6
What is the building block of the exocrine pancreas?
The acinus
Question 7
What are acinar cells responsible for?
Enzymatic secretions: - Synthesize pancreatic enzymes - store zymogens in secretory granules
Question 8
What are ductal cells
produce aqueous secretions in the pancreas and help neutralize acidic stomach contents
Question 9
What are the zymogens secreted by acinar cells for protein digestion?
Trypsinogen, chymotrypsinogen, and procarboxypeptidase.
Question 10
What is the role of enterokinase in protein digestion?
protease found in the duodenum that activates trypsinogen to yield trypsin • Activated trypsin activates chymotrypsinogen and procarboxypeptidase • yields chymotrypsin and carboxypeptidase
Question 11
Acinar cell role in carbohydrate digestion
pancreatic amylase, secreted in the active form
Question 12
Acinar cell role in lipid digestion
pancreatic lipase, secreted in the active form
Question 13
Acinar role in nucleic acid digestions
deoxyribonucleases and ribonucleases are produced to digest the DNA and RNA, respectively
Question 14
What is the role of bicarbonate in pancreatic ductal cell secretions?
Bicarbonate facilitates chloride ion transport across the ductal cell membrane.
Bicarbonate regulates blood glucose levels by enhancing insulin secretion.
Bicarbonate emulsifies dietary fats to aid in digestion.
Bicarbonate neutralizes gastric acid and provides an optimal pH for pancreatic enzymes to function.
Question 15
How do chloride and bicarbonate concentrations in ductal secretions vary with pancreatic flow rate?
high flow rates: Higher bicarbonate and lower chloride
Question 16
What are the three phases of pancreatic secretion regulation?
- cephalic phase via vagal stim - gastric phase via vagal stim and secretin - intestinal phase via CCK, secretin, and vagal stim
Question 17
What is the strongest stimulator for pancreatic secretions?
Intestinal phase • CCK = major for enzyme rich secretions • secretin = water and bicarbonate
Question 18
What is the multiplicative effect in pancreatic secretion?
total secretion is greater than the sum of the secretions caused by each stimulus separately - combined effects of multiple basic stimuli > sum of their individual effects
Question 19
What is the inhibitor of pancreatic secretion?
peptide YY - secreted by neuroendocrine cells in the ileum - decreases pancreatic secretions
Question 20
What are the five different cell types in the endocrine pancreas and what hormones do they secrete?
- Beta → insulin (Abundant) - Alpha → glucagon - Delta → somatostatin - Gamma → pancreatic polypeptide - Epsilon → ghrelin
Question 21
What is the precursor of glucagon?
Proglucagon; synthesized by a cells in pancreas
Question 22
What enzyme is responsible for converting proglucagon into glucagon?
Prohormone convertase 2 (PC2)
Question 23
What is the physiological role of glucagon?
catabolic hormone; elevates blood sugar levels to glucose homeostasis.
Question 24
What are the stimuli that regulate glucagon secretion?
Stimuli: hypoglycemia, exercise, norepinephrine and Ach Inhibitors: insulin, somatostatin, amylin
Question 25
What is the primary function of the alpha cell in the pancreas?
secretes glucagon, helps regulate blood glucose
Question 26
Effects of glucagon on the brain
decreases food intake + appetite, and increases satiety
Question 27
Effects of glucagon on the pancreas
• ↑ insulin secretion
Question 28
Effects of glucagon on the liver
• increase glucose production, lipid breakdown, ketone production, amino acid breakdown • decrease glucose breakdown, lipid production
Question 29
Effects of glucagon on brown adipose tissue
increase resting energy expenditure; will increase weight loss
Question 30
effects of glucagon on the heart
increase heart rate and contractility
Question 31
What is the function of Somatostatin?
secreted by the delta cells of the pancreas - inhibits the secretion of insulin, glucagon, and gastrin
Question 32
Function of pancreatic polypeptide
- Secreted by gamma (PP) cells - Regulates endocrine and exocrine function of pancreas
Question 33
Functions of Ghrelin
- Secreted by epsilon cells - stimulates appetite and release of growth hormone
Question 34
Function of amylin
- stored in β-cell granules, released with insulin - helps suppress secretion of glucagon and slows gastric emptying
Question 35
What is the structure of proinsulin?
Proinsulin consists of three peptide chains: A chain, B chain, and connecting peptide (C peptide).
Question 36
How is the endogenous insulin level determined?
determined by detecting the C-peptide level
Question 37
What is the role of SGLT-1 in glucose transport?
sodium-dependent transporter, transfers glucose from the intestinal lumen into the intestinal mucosa
Question 38
What is the role of GLUT-2 in glucose transport?
sodium-independent transporter, transports glucose through cell's membrane into paracellular space and then into blood
Question 39
What is GLUT2 and what does it do?
moves glucose into beta cells, increasing the ATP/ADP ratio
Question 40
What is the effect of increased ATP/ADP ratio on insulin release?
increase in intracellular calcium concentration → triggers the fusion of insulin secretory granules + plasma membrane → insulin release
Question 41
What are the factors that increase insulin secretion?
• ↑ blood glucose • ↑ amino acids (arginine, lysine, leucine) • ↑ fatty acids • Glucagon • GIP • ACh
Question 42
What are the factors that decrease insulin secretion?
• ↓ blood glucose • Somatostatin • Norepinephrine + epinephrine
Question 43
What is the role of insulin in carbohydrate metabolism?
promotes glucose uptake into cells, enhances glycolysis, and stimulates glycogen synthesis
Question 44
What are the key steps in insulin signaling?
Insulin binds to insulin receptors → phosphorylation of signaling proteins → translocation of GLUT-4 to the plasma membrane → regulation of protein synthesis
Question 45
Expression/Function of GLUT-1
E: skeletal muscle and fat F: Glucose uptake by skeletal muscle and fat under basal conditions
Question 46
Expression/Function of GLUT-2
E: Pancreatic B-cells, liver, intestine, kidney F: ensures glucose uptake only when glucose levels are high
Question 47
Expression/Function of GLUT-3
E: Neurons F: Works with GLUT-1; allowing glucose to cross BBB and enter neurons
Question 48
What is the primary function of GLUT-4?
Major insulin-responsive glucose transporter
Question 49
Where is GLUT-4 predominantly expressed?
Striated muscle and adipose tissue
Question 50
What is the primary mediator of insulin-stimulated glucose uptake?
GLUT-4
Question 51
How does exercise affect insulin receptors?
Exercise upregulates the number of insulin receptors.
Question 52
How does insulin effect carbohydrate metabolism?
S: glucose transport, rate of glycolysis, glycogen synthesis I: glycogen breakdown, gluconeogenesis
Question 53
How does insulin effect lipid metabolism?
S: FA and triacylglycerol synthesis, uptake of triglycerides, rate of cholesterol synthesis I: lipolysis, FA oxidation, ketogenesis
Question 54
Insulin effects on protein metabolism
S: amino acid transport, protein synthesis I: protein degradation, urea formation
Question 55
What is the common cause of acute pancreatitis in adults?
Alcoholism
Question 56
What is the common cause of chronic pancreatitis in children?
Cystic fibrosis
Question 57
What is acute pancreatitis
- activation of pancreatic enzymes → pancreatic autodigestion - sudden-onset epigastric abdominal pain + anorexia/nausea
Question 58
What is chronic pancreatitis
repeated episodes of acute inflammation → fibrosis and damage - persistent pain, worsened by fatty meals or alcohol
Question 59
Complications of Pancreatitis
• steatorrhea • weight loss, deficiencies of fat-soluble vitamins (A, D, E, and K) • Long term: diabetes and pancreatic cancer
Question 60
What percentage of the US population has diabetes?
11.6%
Question 61
How many people have prediabetes in the US?
97.6 million; 38% of US adults
Question 62
What are the increased risks associated with diabetes?
CVD, kidney failure, and nonalcoholic fatty liver disease
Question 63
What is the goal of screening asymptomatic adults for prediabetes and type 2 diabetes?
earlier detection, diagnosis, and treatment, with the ultimate aim of improving health outcomes
Question 64
Diagnostic criterion for Diabetes Mellitus based on HbA1c?
HbA1c ≥ 6.5%
Question 65
Diagnostic criterion for Diabetes Mellitus based on Fasting Plasma Glucose (FPG)?
FPG ≥ 126 mg/dL - fasting is defined as no caloric intake for at least 8 hours.
Question 66
What is the definition of Glycated hemoglobin (A1C)?
Glycated hemoglobin (A1C) is a measure of average blood glucose levels over the past 2-3 months, as around 3% of hemoglobin in circulating red blood cells (RBCs) becomes glycated during their lifespan.
Question 67
HbA1C Levels
• Normal: <5.6% • Prediabetic: 5.7-6.4 • Diabetic: >6.5
Question 68
Fasting plasma glucose Levels
After 8 hours fasting • Normal: 70-100 mg/dL • Diabetic: >126 mg/dL
Question 69
Non-fasting or Random glucose test levels
Any time, pt is symptomatic • Normal: <140 mg/dL
Question 70
What is the Two-hour oral glucose tolerance test (OGTT)?
measures plasma glucose level before and at different time points following the glucose solution ingestion
Question 71
What are the normal and diabetic ranges for the OGTT in mg/dL?
• Normal: <140 mg/dL • DIabetic: >200 mg/dL
Question 72
What is the etiology of Type 1 Diabetes Mellitus?
autoimmune destruction of β-cells, leading to insulin deficiency
Question 73
What percentage of diabetic patients have Type 1 Diabetes Mellitus?
10% of diabetic patients have Type 1 Diabetes Mellitus.
Question 74
What are the two main factors contributing to the pathophysiology of Type 1 Diabetes Mellitus?
Genetic: HLA gene (HLA-DR3 and DR4) mutations Environmental: “accelerators” of beta cell autoimmunity, viral infections, infant nutrition and hygiene
Question 75
What is the histological finding in the absence of insulin immunostaining?
due to β-cells destruction and leukocyte infiltration of islets
Question 76
What is the onset age range for diabetes TI diagnosis?
younger than 30 years old, with a peak diagnosis age around 13-14 years old.
Question 77
What percentage of insulin-secreting beta cells must be destroyed for diabetes symptoms to become obvious?
Diabetes symptoms become obvious when 80% to 90% of the insulin-secreting beta cells are destroyed.
Question 78
Diabetes Type 1 Pathophysiology
- Hypoinsulinemia → increase in glucagon secretion - Decreased amylin → increase of glucagon levels - Glucagon → stimulate glycogenolysis and gluconeogenesis → increase in blood glucose level
Question 79
Clinical symptoms of T1D
• polydipsia • polyuria • polyphagia • weight loss • fatigue
Question 80
Rationale for polydipsia in T1DM
Polydipsia: increased thirst - elevated blood glucose levels → osmotic dehydration and hypothalamic stimulation of thirst
Question 81
Rationale for polyuria in T1DM?
Polyuria: frequent urination - hyperglycemia = osmotic diuretic → kidneys filter more glucose than can be reabsorbed → glycosuria
Question 82
What is the key difference between Type 1 and Type 2 Diabetes Mellitus?
T1D: body's inability to produce insulin T2D: body's tissues not responding to insulin, despite body producing it
Question 83
What is the etiology of Type 2 Diabetes Mellitus?
Multifactorial; genetic susceptibility, insulin resistance, obesity, inadequate insulin secretion
Question 84
What is the prevalence of Type 2 Diabetes Mellitus?
Affect around 90% of the diabetic population.
Question 85
What is insulin resistance?
subnormal cellular response to normal insulin conc. → abnormal glucose metabolism, fatty liver, skin pigmentation, inflammation, and increased risk for conditions like CKD, CVS, and PCOS.
Question 86
How does the pancreas respond to insulin resistance?
pancreas upregulates insulin production to match the hyperglycemic load - can lead to amyloid polypeptide buildup and aggregation in the islets
Question 87
What is compensatory hyperinsulinemia?
body produces excess insulin to counteract the effects of insulin resistance - prevents clinical appearance of diabetes for many years
Question 88
What happens to beta cell function in diabetic patients over time?
overburdening of the beta cell mass → decrease in beta cell function over time → deficiency of insulin
Question 89
What are the clinical manifestations of type 2 diabetes?
nonspecific; fatigue, pruritus, recurrent infections, visual changes, neuropathy-related symptoms, acanthosis nigricans, and polyuria, polydipsia, and weight loss
Question 90
What is acanthosis nigricans?
brownish pigmentation due to insulin resistance and insulin-mediated IGF-1 activation in keratinocytes
Question 91
What is the management strategy for Type 1 diabetes?
exogenous insulin to compensate for endogenous insulin deficiency
Question 92
What is the first-line management strategy for Type 2 diabetes?
First line: diet and exercise to attain a healthy body weight Combo of anti-hyperglycemic meds
Question 93
What is the blood glucose level that defines hypoglycemia?
Blood glucose <70 mg/dL
Question 94
What are the symptoms of autonomic system activation associated with hypoglycemia?
Palpitations, sweating, shaking, nausea, hunger
Question 95
What are the neuroglycopenic symptoms associated with hypoglycemia?
• focal neurological deficit • mental confusion • coma
Question 96
What is Diabetic Ketoacidosis (DKA)?
T1D; insulin deficiency, increased glucagon levels, and the accumulation of acidic ketone bodies, leading to metabolic acidosis
Question 97
What are the key pathophysiological steps in DKA?
decreased insulin → glucagon ratio → promoting lipolysis → increased fatty acid production → conversion of fatty acids to ketone bodies → hepatic output of ketone bodies
Question 98
What are the symptoms of DKA (Diabetic Ketoacidosis)?
Nausea/vomiting, thirst/polyuria, abdominal pain, and shortness of breath (kussmaul breathing).
Question 99
What are the precipitating events for DKA?
inadequate insulin administration, infection, infarction, pancreatitis, drugs (cocaine), and pregnancy
Question 100
Management of DKA
• IV fluids to replenish the lost fluids • administration of insulin & electrolyte monitoring
Question 101
What is the definition of Diabetic Ketoacidosis?
a life-threatening medical condition caused by severe hyperglycemia in the absence or deficiency of insulin, requiring hospitalization due to ketonemia >1.5 mmol/L, ketonuria, and hyperglycemia
Question 102
What is Ketosis and how does it differ from Diabetic Ketoacidosis?
an increase in ketone bodies concentration, from keto or low carbohydrate diet/fasting - Differs: not life-threatening and does not require hospitalization
Question 103
What is the pathophysiology of HHNKS?
insulin deficiency → ↓ glucose uptake (but ↓ lipolysis maintained) → severe hyperglycemia → ↑ plasma osmolarity → glycosuria → osmotic diuresis (polyuria) → severe dehydration + electrolyte loss → neurologic dysfunction → coma/death
Question 104
What are the precipitating events for HHNKS?
Incompliance with treatment and infections.
Question 105
What is the onset of the HHNKS?
Few days-few weeks
Question 106
Symptoms of HHNKS
- partial and complete lack of consciousness - seizures, coma, death
Question 107
What are the long-term complications of diabetes?
- microvascular: eye, kidney, and nerves - macrovascular: brain, heart, and extremities
Question 108
What is neuropathy in the context of diabetes?
damage to the peripheral nervous system caused by hyperglycemia, leading to pain, numbness, and slow-healing foot wounds
Question 109
What is the effect of hyperglycemia on the risk of infections?
Hyperglycemia increases the risk for infections due to impaired immune responses and slower wound healing.
Question 110
Hyperglycemia + Infection risks are attributed to
• hypoxia • decreased blood supply • recurrent infections • impairment of innate and adaptive immune systems • slower collagen synthesis and decreased angiogenesis
Question 111
What are the key factors contributing to xerostomia and hyposalivation in diabetes mellitus patients?
• Damage to salivary gland parenchyma • alterations in salivary gland microcirculation • dehydration • mitochondrial dysfunction
Question 112
Diabetes+ xerostomia complications
caries, damage to the gingiva and supporting tissues, increased risk for infection
Question 113
What is the two-way relationship between diabetes and periodontal disease?
• Damage to the gingiva and supporting tissues is more extensive • treating periodontal diseases may improve glycemic control
Question 114
What is Gestational Diabetes Mellitus (GDM)?
transient form of diabetes that occurs during pregnancy due to increased insulin resistance
Question 115
What is the prevalence of GDM compared to Overt Diabetes?
GDM is more common (80%) compared to Overt Diabetes (15-20%).
Question 116
What is the pathophysiology of gestational diabetes?
• exact mechanism is unknown • insulin resistance, inadequate insulin secretion, and pregnancy hormones are contributing factors
Question 117
What are the complications of gestational diabetes?
• Hyperglycemia and excessive fetal growth → increase the risk of maternal morbidity • 3rd trimester pregnancy loss/stillbirth • fetal complications.
Question 118
What is Diabetes Insipidus?
excretion of abnormally large volumes of dilute urine without an elevated blood sugar level
Question 119
What are the symptoms of Diabetes Insipidus?
polyuria (2-20 L/d) and polydipsia
Question 120
What are the two types of Diabetes Insipidus?
• Central diabetes insipidus: deficient secretion of anti-diuretic hormone (ADH) • Nephrogenic diabetes insipidus: renal resistance to the anti-diuretic hormone