Endocrine System3 Slides 106-155

1. What is the main function of the endocrine pancreas?

Regulates blood pressure through the release of aldosterone

Stores excess glucose in the form of glycogen

ISLETS OF LANGERHANS--SECRETE HORMONES GLUCAGON AND INSULIN--4 CELLS THAT SECRETE HORMONES INTO BLOOD:1. ALPHA CELLS: GLUCAGON2. BETA CELLS: INSULIN3. DELTA CELLS: SOMATOSTATIN (GHIH): WHICH DECREASES GASTRIC SECRETIONS AND EMPTYING, INHIBITS RELEASE OF GASTRIN, INSULIN AND GLUCAGON4. F CELLS: PACREATIC POLYPEPTIDE (REGULAR PANCREATIC SECREATION INDUCED BY HYPOGLYCEMIA)

Produces digestive enzymes for breaking down food

The endocrine pancreas is responsible for secreting hormones such as glucagon and insulin, which play a key role in regulating blood sugar levels.

Explanation

The endocrine pancreas is responsible for secreting hormones such as glucagon and insulin, which play a key role in regulating blood sugar levels.

2. What triggers the release of insulin?

Fasting decreases the levels of amino acids responsible for triggering insulin release

Low levels of cortisol promote insulin secretion

-SECRETION IS PROMOTED BY INCREASED BLOOD GLUCOSE LEVELS: HYPERGLYCEMIA
-FACILITATES RATE OF GLUCOSE UPTAKE INTO CELLS OF BODY
-ANABOLIC HOMRONE THAT INDUCES SYNTHESIS OF PROTEINS, LIPIDS, AND NUCLEIC ACIDS
-MITOGENIC, MEANING IT PROMOTES DNA SYNTHESIS SUCH AS GROWTH AND DIFFERENTIATION
-TRIGGERS THAT RELEASE INSULIN ARE: 1. INCREASED LEVELS OF GLUCAGON2. INCREASED CORTISOL LEVELS3. INCREASED LEVELS OF CERTAIN AMINO ACIDS4. VAGAL STIMULATION 5. CONDITIONS ASSOCIATED WITH INCREASED BLOOD INSULIN LEVELS AND DECREASED PERIPHERAL TISSUE INSULIN RECEPTOR BINDING (OBESITY, HIGH DIETARY CARB INTAKE, CORTISOL)6. CONDITIONS ASSOCIATED WITH DECREASED BLOOD INSULIN LEVELS AND INCREASED PERIPHERAL TISSUE INSULIN RECEPTOR BINDING (EXERCISE AND FASTING)
1. IN RESPONSE TO HIGH GLUCOSE LEVELS, GLUCOSE ENTERS BETA CELLS BY GLUCOSE TRANSPORTER2. GLUSOE IS PHOS AND METABOLIZED TO ATP3. ATP CLOSES K+ CHANNELS DEPOLARIZING CELL4. INDUCES CA2+ CHANNELS TO OPEN TRIGERRING INSULIN RELEASE5. BIPHASIC RELEASE: 1) STORED INSULIN 2) NEW SYNTHESIZED INSULIN
FUNCTION:1. PROMOTES STORAGE OF INGESTED NUTRIENTS2. DECREASES BLOOD GLUCOSE LEVELS BY INCREASING GLUCOSE TRANSPORTERS ON SKELETAL MUSCLE AND ADIPOSE TISSUE--GLUT-4: INSULIN-DEPENDENT GLUCOSE TRANSPORTER--INSULIN-GLUT 4 COMPLEX-->UP TO 20 TIMES INCREASE IN GLUCOSE TRANSPORT RATE--GLUT 1-3 AND 5 GLUCOSE TRANSPORTERS ARE USED BY OTHER TISSUES THAT DO NOT USE GLUT-4: -GLUT-2 MAIN TRANSPORTER INTO BETA CELLS AND LIVER CELLS -RELATIVE LOW AFFIRMITY FOR GLUCOSE--ONLY TRANSPORTS WHEN PLASMA LEVELS ARE HIGH AFTER MEALS -GLUT-1 PRESENT IN ALL TISSUES SUCH AS NERVOUS SYSTEM
GLUT-4 INSULIN DEPENDENT GLUCOSE TRANSPORTER:--GLUT 4-SKELETAL MUSCLE AND ADIPOSE TISSUE CELLS--SEQUESTERED INSIDE MEMBRANE (NON FUNCTIONAL)--INSULIN BINDING: SIGNALS MOVMENT OF GLUT 4 INTO CELL MEMBRANE WHERE IT FACILITATES GLUCOSE ENTRY
INSULIN RECEPTOR BINDING:INSULIN RECEPTOR=2 SUBUNITS (ALPHA-->INSULIN BINDING, BETA-->KINASE DOMAIN)
INSULIN BINDING CAUSES AUTOPHOSPHORYLATION OF BETA SUBUNIT-->TYROSINE KINASE ACTIVITY-->SIGNALING CASCADE

Glucagon helps reduce insulin release

3. What is the target organ of glucagon and what are its effects?

Muscles are the target organ of glucagon where it promotes protein synthesis.

Pancreas is the target organ of glucagon and it increases insulin secretion.

LIVER IS TARGET ORGAN OF GLUCAGON (ALPHA CELLS)--TRAVELS THROUGH PORTAL CIRCULATION (LIKE INSULIN)--PROMOTES GLUCOGENESIS AND GLYCOGENOLYSIS -INCREASES BLOOD GLUCOSE
IT CAUSES DECREASED LIPOGENESIS, INCRESAED LIPOLYSIS, KETOGENESIS, PROTEOLYSIS
SOMATOSTATIN (GHIH) (DELTA CELLS)--POLYPEPTIDE HORMONE, 14 AA, SHORT HALF LIFE--INVOLVEMENT IN REGULATING ALPHA AND BETA CELL SECRETIONS--DECREASES GI ACTIVITY, INCREASES USE OF ABSORBED NUTRIENTS
TRIGGERS THAT RELEASE GLUCAGON:PROMOTED BY DECREASED BLOOD GLUCOSE LEVELS: HYPOGLYCEMIA SUCH AS BETWEEN MEALS, EXERCISE, STARVATION, DECREAED INSULIN, ETC

Adipose tissue is the target organ of glucagon and it decreases blood glucose levels.

Glucagon primarily targets the liver to increase blood glucose levels by promoting glycogenolysis and gluconeogenesis.

Explanation

Glucagon primarily targets the liver to increase blood glucose levels by promoting glycogenolysis and gluconeogenesis.

4. Which hormones affect blood glucose levels?

Cortisol and adrenaline

Testosterone and progesterone

Estrogen and melatonin

Insulin and glucagon are two of the main hormones that regulate blood glucose levels in the body. Insulin helps lower blood sugar levels by facilitating the uptake of glucose into cells, while glucagon helps increase blood sugar levels by promoting the breakdown of glycogen in the liver.

Explanation

Insulin and glucagon are two of the main hormones that regulate blood glucose levels in the body. Insulin helps lower blood sugar levels by facilitating the uptake of glucose into cells, while glucagon helps increase blood sugar levels by promoting the breakdown of glycogen in the liver.

5. What is diabetes mellitus?

A type of cancer affecting the bones.

METABOLIC DISEASE CHARACTERIZED BY HYPERGLYCEMIA DUE TO LACK OF INSULIN PRODUCTION OR SENSITIVITY
DISORDER OF CARBOHYDRATE, LIPID, AND PROTEIN METABOLISM
TYPE 1: INSULIN DEPENDENTTYPE 2: NON INSULIN DEPENDENTSECONDARY DMGESTATIONAL DM
DIAGNOSTICS-POLYDIPSIA AND POLYURIA-WEIGHT LOSS (IDDM ONLY)-OBESITY (NIDDM ONLY)-FASTING VENOUS BLOOD GLUCOSE >140MG/DL=7.8MM
-ORAL GLUCOSE TOLERANCE TEST (OGTT)*PERFORMED IN BORDERLINE CASES---IMPAIRED GLUCOSE TOLERANCE -GIVEN 75G ORAL GLUCOSE LOAD, AFTER 2 HOUR, BLOOD GLUCOSE >140MGDL OR ANYTIME >200MG/DL
--GLYCOHEMOGLOBIN (hbA1c test) -MEASURES NON ENZYMATIC GLYCOSYLATION OF HEMOGLOBIN -INDICATES SUCCESS OF LONG TERM BLOOD GLUCOSE CONTROL

A neurological disorder affecting the spinal cord.

A condition characterized by low blood sugar levels.

Diabetes mellitus is a metabolic disease characterized by high blood sugar levels, often due to lack of insulin production or insensitivity. It is not related to cancer, neurological disorders, or low blood sugar levels.

Explanation

Diabetes mellitus is a metabolic disease characterized by high blood sugar levels, often due to lack of insulin production or insensitivity. It is not related to cancer, neurological disorders, or low blood sugar levels.

6. What is the mechanism of ketoacidosis?

Overdose of epinephrine leading to hypoglycemia

Excessive stress leading to cortisol deficiency

INSULIN DEFICIENCY-->EPINEPHRINE-->RELEASE OF GLUCAGON
GLUCAGON:-STIMULATES GLUCOGENESIS-->HYPERGLYCEMIA-->OSMOTIC DIURESIS-->DEHYDRATION
-BREAKDOWN OF ADIPOSE TISSUE-->FATTY ACIDS CONVERTED TO FATTY ACETYL Co A in liver-->OXIDIZED BY LIVER MITOCHONDRIA TO KETONE BODIES-->KETONEMIA AND KETONEURIA-->METABOLIC KETOACIDOSIS
KETOACIDOSIS TRIGGERED BY:INSULIN DEFIENCIECY (eg: IDDM)LOW CARB DIET DUE TO HYPOGLYCEMIA TRIGGERING GLUCAGON RELEASESTRESS OR ILLNESS: ANTI-STRESS HORMONES (CORTICOL, EPINEPHRINE, GH) OPPOSE INSULIN AND TRIGGER GLUCAGON RELEASE
MECHANISM OF KETOACIDOSIS-LACK OF INSULIN INDUCES RELEASE OF GLUCAGON RELEASE BY ALPHA CELLS-->HEPATIC EFFECTS --increased glucogenesis --increased glycogenolysis --impaired glucose utilization by liver --increased amino acid uptake by liver --increased ketone body formation (ketogenesis):incomplete oxidation of free fatty acids
-ACETONE -ACETONACETIC ACID -BETA-HYDROXYBUTRYIC ACID -->KETOACIDOSIS=METABOLIC ACIDOSIS
SIGNS AND SYMPTOMS:VOLUME DEPLETION (INCREASED OSMOTIC PRESSURE IN TUBULE-->OSMOTIC DIURESIS)-HYPOTENSION--------DRY SKINAND PULSE-WEAK RAPID PULSE-ODOR OF ACETONE ON BREATH-HYPERGLYCEMIA-MAY PROGRESS TO COMA-INSULIN SHOCK (HYPOGLYCEMIA DUE TO INSULIN OVERDOSE) CAN LEAD TO COMA-DISTINGUISH BETWEEN DIABETIC (KETOTIC) COMA VS. INSULIN SHOCK COMA----NO VOLUME DEPLETION, NORMAL BLOOD PRESSURE, MOIST SKIN, HYPGLYCEMIA

High carb diet leading to excessive insulin production

7. What is the primary pathology related to Type 2 Diabetes Mellitus?

-Excessive production of insulin by the pancreas

-Autoimmune destruction of pancreatic beta cells

-Impaired production of glucagon by the liver

-NON INSULIN DPENDENT DIABETES, ADULTS ONSET DM (>30 YEARS)
-PRIMARY DIABETES-->PATHOLOGY RELATED TO INABILITY OF PERIPHERAL TISSUES TO RESPOND TO INSULIN---LEADS TO DECREASED GLUCOSE UPTAKE AND INABILITY TO SUPPRESS GLUGOGENESIS-OBESITY AND GENETIC FACTOR-NORMAL OR INCREASED BLOOD INSULIN
ETIOLOGY-GENETICALLY DEFECTIVE INSULIN RECEPTORS OR SIGNALLING-OBESITY: TRIGLYCCERIDES AND HORMONES INTERRUPT INSULIN SIGNALLING-B CELL DYSFUNCTION
PATHOGENESISPERIPHERAL INSULIN RESISTANCE
MECHANISM:-ABNORMAL BETA CELL INSLUIN RELEASE UPON PANCREATIC STIMULATION-DECREASED NUMBER OF CELL SURFACE INSULIN RECEPTORS-POST RECEPTOR DEFECT (INSULIN BINDING FAILS TO INDUCE INSERTION OF GLUT4 INTO MEMBRANE)-DECREASED NUMBER OF GLUT4 TRANSPORTERS
SIGNS AND SYMPTOMS:-PERIPHERAL INSULIN RESISTANCE-NORMAL OR INCREASED BLOOD INSULIN-NO ISLET CELL AUTO-ANTIBODIES-NO KETOACIDSOS-CENTRAL OBESITY-GENETICS
TREATMENT
-EXERCISE-WEIGHT REDUCTION-DIETARY RESTRICTION (OF REFINED CARBS AND CALORIES)-ORAL HYPOGLYCEMIC OR EUGLYCEMIC AGENTS-INSULIN INJECTIONS

Type 2 Diabetes Mellitus is characterized by peripheral tissues' inability to respond effectively to insulin, leading to decreased glucose uptake and increased gluconeogenesis.

Explanation

Type 2 Diabetes Mellitus is characterized by peripheral tissues' inability to respond effectively to insulin, leading to decreased glucose uptake and increased gluconeogenesis.

8. Compare Type 1 and Type 2 DM.

Identify the similarities between Type 1 and Type 2 DM.

Contrast the differences between Type 1 and Type 2 DM.

Discuss the treatment options for Type 1 and Type 2 DM.

Type 1 diabetes is an autoimmune condition where the body attacks insulin-producing cells, whereas Type 2 diabetes is often linked to lifestyle factors such as diet and exercise. Type 1 diabetes usually requires insulin injections for treatment, while Type 2 diabetes can sometimes be managed with lifestyle changes and oral medications.

Explanation

Type 1 diabetes is an autoimmune condition where the body attacks insulin-producing cells, whereas Type 2 diabetes is often linked to lifestyle factors such as diet and exercise. Type 1 diabetes usually requires insulin injections for treatment, while Type 2 diabetes can sometimes be managed with lifestyle changes and oral medications.

9. What is secondary diabetes mellitus?

HYPERGLYCEMIA ASSOCIATED WITH IDENTIFIABLE CAUSES OF ISLET DESTRUCTION SUCH AS PANCREATITIS, SURGERY, TUMOURS, HEMOCHROMATOSIS VIA PANCREATIC DAMAGE
OR
HYPERGLYCEMIA ASSOCIATED WITH DRUGS OR HYPERSECRETED HORMONES WITH ANTAGONIZE INSULIN ACTION SUCH AS GLUCOCORTICOSTERIODS, hGH, ADRENERGIC AGONISTS OR CORTISON IN CUSHING'S, GH IN ACROMEGALY, ADRENALIN

Gestational diabetes mellitus occurring during pregnancy due to hormonal changes.

Type 2 diabetes caused by insulin resistance and inadequate insulin production.

Type 1 diabetes caused by genetics and autoimmune factors.

Secondary diabetes mellitus refers to hyperglycemia associated with specific identifiable causes, rather than the typical genetic or lifestyle factors seen in primary diabetes types. It is important to distinguish these different forms of diabetes for proper diagnosis and treatment.

Explanation

Secondary diabetes mellitus refers to hyperglycemia associated with specific identifiable causes, rather than the typical genetic or lifestyle factors seen in primary diabetes types. It is important to distinguish these different forms of diabetes for proper diagnosis and treatment.

10. What are some long-term complications of poorly controlled diabetes mellitus?

Eczema

-NEPHROPHATHY-NEUROPATHY-RETINOPATHY-VASCULAR DISEASE-IMMUNODEFICIENCY-ATHEROSCLEROSIS

Hypertension

Osteoporosis

The correct long-term complications of poorly controlled diabetes mellitus include nephropathy, neuropathy, retinopathy, vascular disease, immunodeficiency, and atherosclerosis. Hypertension, osteoporosis, and eczema are not directly associated with poorly controlled diabetes mellitus.

Explanation

The correct long-term complications of poorly controlled diabetes mellitus include nephropathy, neuropathy, retinopathy, vascular disease, immunodeficiency, and atherosclerosis. Hypertension, osteoporosis, and eczema are not directly associated with poorly controlled diabetes mellitus.

11. What are the 3 pathways through which hyperglycemia causes blood vessel lesions?

1. Lipid oxidation, 2. DNA methylation, 3. Cytokine production

1. PROTEIN GLYCOSYLATION-GLUCOSE IN CELL FORMS BYPRODUCT THAT COMBINES AMINO GROUPS OF PROTEINS PRODUCING "ADVANCED GLYCATION END PRODUCTS" (AGE)
-AGE DESTROYS ECM, MODIFIES CIRCULATING PLASMA PROTEINS WHICH THEN DESTROY ENDOTHELIAL, MESANGIAL AND MACROPHAGE CELLS
-LEADS TO ATHEROGENESIS AND MICROVASCULAR INJUY

2. INTRACELLULAR HYPERGLYCEMIA IN NON-GLUT4 CELLS
-DISTURBS ANTIOXIDANT PATHWAYS AND CAUSES TISSUE DAMAGE:---DEPLETION OF NADPH-->DECREASED GLUTHIONINE (DECREASED ANTI-OXIDANT CAPACITY)---HIGH GLUCOSE-->GLUCOSE IS CONVERTED TO SORBITOL AND FRUCTOSE -SORBITOL AND FRUCTOSE INCREASE INTRACELLULAR OSMOLARITY -INFLUX OF WATER -CELL INJURY AND POSSIBLE CELL DEATH
3. ACTIVATION OF PKC
-PKC IS ACTIVATED BY EXCESS CA2+ (WHICH IS ACTIVATED BY GLUCOSE): WHICH CAUSES
-PROANGIOGENESIS-->RETINOPATHY-INACTIVATION OF eNOS(VASODILATOR) AND INCREASES E1 (VASOCONSTRICTOR)-INCREASES PROFIBROGENIC MOLECULES-->ECM DEPOSITION-INCREASES PROCOAGULANT MOLECULES-->VASCULAR OCCLUSIONS-INCRESAES PROINFLAMMATORY CYTOKINES

Hyperglycemia causes blood vessel lesions through the pathways of protein glycosylation, intracellular hyperglycemia in non-GLUT4 cells, and activation of PKC, not through lipid oxidation, DNA methylation, or cytokine production.

Explanation

Hyperglycemia causes blood vessel lesions through the pathways of protein glycosylation, intracellular hyperglycemia in non-GLUT4 cells, and activation of PKC, not through lipid oxidation, DNA methylation, or cytokine production.

12. What is the difference between high blood sugar and low blood sugar?

Low blood sugar is when there is an excess of glucose in the blood, while high blood sugar is when there is a lower than normal level of glucose in the blood.

High blood sugar is a medical emergency, while low blood sugar is not a serious condition.

High blood sugar is when there is lower than normal level of glucose in the blood, while low blood sugar is when there is an excess of glucose in the blood.

High blood sugar (hyperglycemia) can lead to long-term complications for individuals with diabetes, while low blood sugar (hypoglycemia) can cause immediate symptoms and requires prompt treatment to prevent serious health risks.

Explanation

High blood sugar (hyperglycemia) can lead to long-term complications for individuals with diabetes, while low blood sugar (hypoglycemia) can cause immediate symptoms and requires prompt treatment to prevent serious health risks.

13. What may cause syndromes associated with islet cell hyper-function?

Genetic mutations unrelated to islet cell function

Endocrine disorders unrelated to islet cells

Pancreatic islet cell hypofunction

SYNDROMES ASSOCIATED WITH ISLET CELL HYPER-FUNCTION MAY BE CAUSED BY:
-DIFFUSE ISLET CELL HYPERPLASIA-ISLET CELL ADENOMAS-MALIGNANT ISLET CELL TUMORS

Syndromes associated with islet cell hyper-function may be caused by diffuse islet cell hyperplasia, islet cell adenomas, and malignant islet cell tumors.

Explanation

Syndromes associated with islet cell hyper-function may be caused by diffuse islet cell hyperplasia, islet cell adenomas, and malignant islet cell tumors.

14. What is 9999999999999?

999999999999

99999999999

9999999999999999

999999999999999

The correct answer is 999999999999999, which is one trillion minus one. The incorrect answers provided are variations of the correct number, so be careful to choose the answer that is one trillion minus one.

Explanation

The correct answer is 999999999999999, which is one trillion minus one. The incorrect answers provided are variations of the correct number, so be careful to choose the answer that is one trillion minus one.

15. What is the etiopathogenesis of hyperinsulinism?

ETIOPATHOGENESIS-DUE TO ISLET CELL HYPERPLASIA & BETA-CELL TUMORS (INSULINOMAS) -HYPERPLASIA CHARACTERISITC OF INFANTS BORN TO DIABETIC MOTHERS (SUBJECTED TO SUBSTAINED HYPERGLYCEMIA IN UTERO) -MOTHER'S INUSLIN CANNOT CROSS PLACENTAL BARRIER BUT GLUCOSE CAN
ADENOMAS-AFFECTS WOMEN USUALLY
METASTASIZING CARCINOMAS
CAUSES EXCESSIVE INSULI PRODUCTION-->HYPOGLYCEMIC ATTACKS

SIGNS AND SYMPTOMSEXCESS SYMPATHETIC NERVOUS SYSTEM ACTIVITY (SWEATING, PALPITATION, NERVOUSNESS)-CONFUSION, STUPOR, LOSS OF CONCIOUSNESS (TRIGGERED BY FASTING OR EXERCISE)
TREATMENTGLUCOSE ADMINISTERATION (FEEDING OR INFUSION) AND POSSIBLE SURGERY

Caused by excessive insulin intake from diet

Linked to increased cortisol levels in the body

Resulting from a deficiency in pancreatic enzymes

Hyperinsulinism is primarily caused by islet cell hyperplasia and beta-cell tumors, especially in the case of infants born to diabetic mothers. The other incorrect answers do not align with the known causes of hyperinsulinism.

Explanation

Hyperinsulinism is primarily caused by islet cell hyperplasia and beta-cell tumors, especially in the case of infants born to diabetic mothers. The other incorrect answers do not align with the known causes of hyperinsulinism.