Exam 5 Flashcards
What are the functions of Secretin?
Where is it secreted?
What stimulates secretion?
What does it inhibit?
Synthesis: It is a gastrointestinal PEPTIDE HORMONE, Secreted from S-cells of duodenum (secret-tin agent, Snake duo-denim)
Secretion is stimulated by Fatty acids in duodenum (bacon-acid-lemon)
It stimulates pancreatic bocarbonate secretion and bile acid secretion from the liver to help with digestion (Intestinal epethelial passes through pyloric spinchter, senses bolus and signal S-cells to secret it)
Secretin helps start digestion of FATTY ACIDS in the small intestine
It helps decrease gastric acid secretion from the stomach (PARIETAL cells) to prevent excess acid damage to mucosa of dudonum
Bicarbonate secretion occurs in ductal celss of pancreas and Brunner’s glands of duodenum
Bile from liver and stored in gallbladder function to EMULSIFY and ABSORB LIPIDS
What else is absorbed in the stomach, duodenum, jejunum, ileum?
Stomach: water, fluoride, copper, iron, and molybdenum
Duodenum: Iron, folate, FAT SOLUBLE VITAMINS (ADEK), Thiamin, riboflavin, and niacin
(Mycrocitic Anemia: iron deficiency)
(Neural defects, diarrhea, heart problems: Folate deficiency)
Jejunum: Folate, lipids, small peptides, and monosaccharides
Ileum: Vitamin B12 (cobalamin), reabsorption of bile salts and acids. Vitamins C,D,K, folate and magnesium
Vitamin B12: can’t be produced by the body. It is involved in DNA synthesis, and fatty acids synthesis.
(Nervous system impairment peripheral and CNS: VB12 deficiency)
Where can lipids be absorbed through passive diffusion?
Where is calcium absorbed?
Where are the Brunner Glands?
What/where are Prayer’s Patches?
Where is ADEK reabsorbed?
Where is Fe2+ absorbed?
Passive diffusion of lipids in Jejunum
Calcium is absorbed in Small Intestinal wall Jejunum
Brunner Glands are in duodenum, S-secreting cells of submucosa
Prayer’s patches are in Ileum, Lymphoid aggregates in lamina propia.
ADEK: duodenum
Vitamin E deficiency is not absorbed in Ileum too
Vitamin B12 binds to intrinsic factor
What is the fuction (s) of CCK?
Where is it produced/secreted?
What does it stimulate or inhibit?
What does it regulate?
What are the Chief cells and what do they secrete?
What affects does H+ have on stomach digestion, what does it activate?
What are the other two protective substances in the stomach?
What cells produce gastrin and what does this stimulate?
What cells produce Somastostatin and what is its function?
What nerve inhibits Somatostatin?
What neurotransmitter acts in Stomach digestion to stimulate parietal cells?
Chief cells in the stomach secrete PEPSINOGEN (Pimpcinnamon)
Pepsinogen is activated by H+ (HCl) into PEPSIN (protease, digests proteins).
Protein break down starts in the stomach and ends in the duodenum of the small intestine
Mucous cells Secrete mucus and bicarbonate.
Mucus protects the m.m from erosion from acid. HCO3- helps neutralize acids after stomach contents pass on to the small intestine.
G-CELLS secrete GASTRIN, which stimulates further secretions fromt he stomach, such as HCl from PARIETAL cells. Gastrin induces mixing of the contents of the stomach to form an acidic semifluid mixture called CHYME.
Gastrin also increases HISTAMINE release to active PARIETAL cells.
PARIETAL cells secrete INTRINSIC FACTOR, which is required for the absorption of vitamin B12
DELTA cells (found in the antrum of the stomach and in the endocrine pancreas) release SOMATOSTATIN
Somatostatin, if low pH, INHIBITS most GI secretions (e.g., gastric acid, pepsinogen, pancreatic and small intestine fluid secretions, INSULIN, and GLUCANGON release)
Somatostatin is stimulated by increased acid
Inhibited by Vagal stimulation (Ach)
What are the three sections of the small intestine and where does digestion finish?
What enzymes assist in carbohydrates absorption and where are they?
How are pancreatic enzymes secreted?
What does the pancreas secret?
What two proteases are activated by the Brush-border?
What cells secrete mucus and what is its function?
What enzymes break down lipds?
What enzymes break down carbohydrates and DNA/RNA?
Where is bile stored and released?
Duodenum, Jejunum, Ileum
Digestion finishes in the duodenum
Brush-border enzymes are digestive enzymes sitting on the microvilli-covered epethilial cells lining. They are terminal sites for carbohydrates digestion and also assist in absorption.
Pancreatic enzymes are secreted via PANCREATIC DUCT, which is part of the pancreas that connects with the duodenum and carries secretions.
The pancreas secrets bicarbonate through the duct to neutralize acidic CHYME entering from the stomach.
Brush-border enzymes (enterokinase, enteropeptidase) activate pancreatic Trypsin, which activates Chymotripsin. They are PROTEASES that digest protein and break them down into Amino Acids.
The Gallbladder releases LIPASE, which breaks down AAs and free fatty acids.
Goblet cells secret MUCUS in the duodenum, which buffers the acidic CHYME protecting the walls of the duodenum.
Pancreatic AMYLASE breaks down carbohydrates into simple sugars that began breaking down in the mouth.
Pancreatic NUCLEASES break down DNA/RNA molecules, which are absorbed in the Ileum as sugar, base, and phosphate.
What is it, where is secreted, what cells secret it?
What inhibits it and what stimulates it?
What organs and functions does it affect?
What medicine is used as treatment?
Somatostatin is a hormone secreted by D-cells in the pancreas and scattered thoughout the GI mucosa.
It has the primary function of inhibiting GI system by decreasing secretions of gastric acid and pepsinogen, decresing pancreatic and small intestine fluid secretion. It decreases contraction of gallbladder and GLUCAGON and INSULIN secretion.
Somatostatin is upregulated by acid in duodenum and downregulated by Vagal stimulation.
The analog, OCREOTIDE is used in CARCINOID SYMDROME and ESOPHAGEAL VISCERAL BLEEDING.
What is it?
How is it treated?
What does it affect?
What are the symptoms?
It is a condition characterized by by EXCESS secretion of HORMONES and PEPTIDES that act on the GI tract.
SERATONIN and HISTAMINE among other hormones.
The most prominent symptom is the excess secretion of fluids in the GI tract, causing SEVERE DIARRHEA.
OCTREOTIDE can be used to relieve these symptoms due to its inhibitatory effect.
What are they usually related to?
How is it treated?
They are usually related to PORTAL HYPERTENSION.
Backed up bloodflow to liver results in excess dialation of blood vessels where portal and systematic venous systems anastomose, such as esophagus and abdomen and rectum.
Tx: OCTREOTIDE
What is reabsorbed in the large intestine?
What is stored and where?
What vitamins are synthesized in the large intestine?
What makes most of the large intestine?
The large intestine is the last part of the digestive tract that prepares waste excretion.
The majority of the large intestine is the COLON, which is divided in four parts:
Ascending colon, transverse colon, descending colon, and sigmoid colon.
Electrolytes reabsorption, particularly SODIUM and POTASSIUM occurs in the transverse colon.
WATER is reabsorbed throughout the colon
MICROFLORA and helpful bacteria produce vitamins, including Vitamin K and B
The RECTUM, which is located before the anus, stores the feces
What organs make part of the foregut?
What is the innervation to these organs?
What artery supplies blood to these structures?
Esophagus, Stomach, Proximal duodenum, Liver, Gallbladder, Spleen, Pancreas.
The VAGUS NERVE (CN X) and ENTERIC NERVE SYSTEM innervates the foregut structures. It provides parasympathetic innervation to these and other glands/organ.
What nerves intervate the midgut?
What structures make up the midgut?
The Vagus Nerve and the Splenich Nerve
What structures make part of the hindgut?
What nerves innervate this GI section?
Symphathetic: LUMBAR SPLANCHNIC
Parasympathetic: PELVIC NERVE
Where is bile synthesized?
What is the rate limiting step?
What are the constituents of bile?
Where is it stored?
Where is it secreted?
How is it returned to the liver?
Bile is synthesized continously by hepatocytes of the liver.
The constituents of Bile include, Bile Salts, Cholesterol, Phospholipids, Bilirubin, Ions, and Water.
The rate limiting step is 7 Alpha-hydroxylase, which adds a hydroxyl group to cholesterol
Cholesterol conjugates with amino acids in a later step synthesis, the now conjugated bile-salt has amphipathic properties, allowing emulsification of lipids.
The bile is stored in the Gallbladder.
CCK initiates the release of bile into deudenum. It is relased by I-cells into the Duodenum and Jejunum.
The bile is returned to the liver via Hepatic Portal System.
Nutrients are directly absorbed through the blood in the liver, which allows the recycling of the bile salts.
Bilirubin is a yellow-byproduct of hemoglobin breakdown.
The reticuloendothelial system degrades hemoglobin to produce conjugated bilirubin which is bound to ALBUMIN and transported to the liver, which conjugates the bilirubin and secretes it with bile.
Bile salts are 50% of the organic component of bile. The conjugated cholesterol with amino acids creates micelles around lipids. It aids in the emulsification and digestion of dietary fats.
Ions are secreted by bile ducts along with water, which is stimulated by Secretin.
What are the type of cells in the pancreas and what do they release?
What functions does the pancreas have?
Which are the peptide hormones release in pancreas?
The pancreas is an organ that is involved in both the digestive and endocrine system.
It produces hormones that regulate the body’s blood sugar levels, also releases digestive enzymes into the small intestine.
ACINAR cells release digestive enzymes: ACINI part of the pancreas, EXOCRINE pancreas.
DUCTAL EPETHELIAL cells: release bicarbonate (Aquos) also part of the EXOCRINE pancreas.
INLETs OF LANGERHANS: contain the ALPHA and BETA cells, and it is part of the ENDOCRINE pancreas. Responsible for the regulation of blood sugar levels.
ALPHA cells: release Glucagon
BETA cells: Insulin is senthesized in these cells. 65-80% of the cells in the ENDOCRINE pancreas.
Insulin activates Beta cells and inhibits Alpha cells. It also causes liver cells, skeletal muscles, and fat tissue to absorb glucose and decrease blood sugar levels.
SOMATOSTATIN: pancreatic peptide hormone that inhibits Cholecystokinin, Gastrin, Glucagon, Insulin, and Secretin
SOMATOSTATIN: inhibits alpha and beta cells. Inhibits GROWTH HORMONE and THYROID-STIMULATING HORMONE
Endocrine: release constents to the bloodstream
Exocrine: substances released (e.g., enzymes) travel to another cavity or outside the body. Acinar and Ductal Epethelial cells are part of the endocrine pancreas.
What type or hormone is Glucagon?
What cells make it?
Where is it secreted?
It is a polypeptide hormone made by ALPHA cells of the pancreas.
Glucagon increases the amount of glucose in circulating blood.
Glucagon promotes GLYCOGENOLYSIS (biosynthesis of glycogen to readily avialable glucose) in liver. Glycogen is a form of glucose stored in the liver that converts to glucose when necessary.
Hypoglacemia results from insulin overdose. Glucagon is the treatment for this condition if it is not related to starcation as there is no glycogen stored on liver.
NOREPINEPHRINE releases glucagon.
CALCIUM CHANNELS blockers reversal.
What is the normal range for the anion gap?
What are the causes of Metabolic Alkalosis?
Normal 8-16 mEg/L
The common causes of this abnormality are MUDPILES Methanol, Uremia, Dibetes ketoacidosis, Propelyne glycol, Iron toxicity, Iron or Isoniazid, Lactic Acidosis, Ethelyne glycol, Salicylates.
Methanol is metabolized to FORMIC ACID, which is responsible for ocular toxicity leading to blindness.
Uremia: is a term used to describe RENAL FAILURE due to Nitrogeneous waste buildup in the Blood.
See DKA
Propylene Glycol: is a food additive that is widely used in food and tabacco products, pharmaceuticals, cosmetics. It acts as an emulsifying agent, surfactant, solvent, and drying agent.
Iron or Isoniazid: If ingested in excess can lead to metabolic acidosis. It cal also lead to stomach ulceration. Common symptoms of iron intoxication include: nausea, and vomiting.
What does DKA cause?
What type of dibetes are connected to this disorder?
What happens due to insulin deficiency?
DKA is a life-threatening condition in patients with DIBETES MELLITUS.
It can occur in patients with Type 1 and Type 2 DM
The INSULIN RESISTANCE: stimulates lipoprotein lipase resulting in the breakdown of adipose stores and increased levels of fatty acids oxydation.
The FATTY ACIDS OXIDATION in the hepatic mitochondria produces KETONE BODIES including ACETOACETIC ACID and Beta-Hydroxybutyric acid.
The Ketone Acids can increase the Anion Gap.
What causes metabolic Alkalosis?
Diuretics use LOOP THIAZIDE DIURETICS: ECF Volume contraction causes Increase HCO3 reabsorption, Increase AG2 and Aldosterone
Vomiting: Loss of Gastric H+
Antacid use
Hyperaldosteronism (excess bicarbonate resorption: absorption into the circulation of cells or tissues)
Hypokalemia (secretions of K due to Aldosterone): K+ in cells while H+ in blood bc trying to compensate by INTERCALATED CELLS
What pharmaceuticals can cause Respiratory Acidosis?
What respiratory disorders can cause this?
What PCO2 value is associated with this?
It is characterized by decreased ventilation, which causes increased levels of PCO2 leading to a decrease in blood pH.
Causes: Hypoventilation
Increased PCO2 > 45 mm Hg
Barbiturates: drugs that depress the CNS by increasing the duration of Cl- CHANNELS opening and thus decreasing neuron firing (Hyperpolarized)
What is the most common cause of this acid-base imbalance?
What pharmaceuticals can lead to Respiratory Alkalosis?
It is an acid-base imbalance caused by the decreased CO2 in the blood.
Most often due to HYPERVENTILATION which results is excess loss of CO2
HIGH ALTITUDE causes a person to increase repiratory rate in compensation for the low partial pressure of oxygen inhaled that leads to lower delivery of oxygen.
ASPIRIN or SALICYLATES stimulate the brain stem to increase respiratory rate and ventilation, However, Salicylates can present a mixed acid-base disturbance because they increase the anion gap leading to metabolic acidosis along with respiratory alkalosis.
RESTRICTIVE LUNG DISEASE leads to decrease acquired oxygen bc inability of lungs to expand, to compensate there is an increase in RR leading to respiratory alkalosis.
PULMONARY EMBOLISM occludes the lung vasculature creating dead space within the lung. The body compensates by increasing RR.
PREGNANCY increase PROGESTERONE stimulates brainstem to increase Vm (minute ventilation) thus RR is increased.
RIB FRACTURE decrease lung expansion due to pain on inspiration, the body compensates by increasing RR
ANXIETY increases RR decreases CO2
Hypocalcemia (see metabolic alkalosis) and Hypokalemia (albumin is more Neg charged and binds to Ca2+ thus decreasing serum Ca2+ in free form) are associated with Respiratory Alkalosis as a result of compensation mechanisms. This is temporary until hormonal regulation returns Ca2+ to normal levels.
Fact: Increase in pH can result in HYPOKALEMIA
What medications can be used to treat this disorder?
Cimentidine
Omeprazole
Removal of tumor, as last resort, gastric resection.
What type of signaling do they provide?
What are they made of?
Peptide Hormones are proteins involved in ENDOCRINE system signaling.
They are derived from AAs and can not travel through the cell membrane because they tend to be too large.
They bind to cell membrane receptors, which stimulate secondary messengers, like cAMP, to induce enzymatic changes in the cell. The effects are short-lived because the secondary messenger systems are short-lived and responsive, but also fast-acting, because the effects do not rely on DNA transcription to occur.
Examples of peptide hormones:
Insulin functions to deliver glucose from the bloodstream into muscle, fat, liver and most other cells, allowing the body to use it for fuel.
PTH (used in release of Ca2+ from bones when Calcium levels are low in the blood. Reduce phosphate reabsorption, thus reducing its levels in the blood, and helps Activation of Vitamin D )
ADH (Vasopressin) reabsoprtion of water and Na+
Oxcytosin
How long do they act?
Where do they act?
What are some examples of steroid hormones?
Are they cell membrane permeable?
Where do they bind?
They are cholesterol derived and synthesized in adrenal glands. Used in endocrine function and as neurotransmitters.
They pass through the cell membrane and are slow-acting.
They bind to intracellular receptors and/or intranuclear receptors.
They FIRST affect DNA TRANSCRIPTION and activate certain genes ON/OFF
They are long-lived and slow-acting
Examples of Steroid Hormones
Estrogen
Testosterone
Cortisol decreases bone formation and supresses the immune system. Response to STRESS and LOW BLOOD SUGAR
Aldosterone which controls plasma sodium and has an effect on arterial blood pressure
